hormones of the endocrine system. hormones of the pituitary neurohypophysis--posterior pituitary...
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HORMONES OF THE ENDOCRINE
SYSTEM
HORMONES OF THE PITUITARY
• NEUROHYPOPHYSIS--POSTERIOR PITUITARY
• ADENOHYPOPHYSIS--ANTERIOR PITUITARY
HORMONES OF THE NEUROHYPOPHYSIS
• STORES AND SECRETES NEUROHORMONES PRODUCED BY HYPOTHALAMUS
• ANTIDIURETIC HORMONE
• OXYTOCIN
ANTIDIURETIC HORMONE
• ADH
• VASOPRESSIN
• PREVENTS DIURESIS (LOSS OF URINE)
• CONSTRICTS ARTERIOLES AND RAISES BLOOD PRESSURE
• SYNTHESIZED IN SUPRAOPTIC NUCLEI OF HYPOTHALAMUS
• CARRIED IN HYPOTHALAMOHYPOPYSEAL TRACT
• STORED IN AXON TERMINALS IN PITUITARY
ANTIDIURETIC EFFECT
• AFFERENT VAGAL NERVES
• DROP IN PRESSURE STIMULATES ADH SECRETION
• INCREASE IN PRESSURE INHIBITS SECRETION
FACTORS THAT INCREASE ADH SECRETION
• EMOTIONAL STRESS• PHYSICAL STRESS • BLOOD VOLUME• INCREASED PLASMA OSMOTIC PRESSURE• DECREASED EXTRACELLULAR FLUID
VOLUME• STRENUOUS EXERCISE• NICOTINE AND BARBITUATES
FACTORS THAT DECREASE ADH SECRETION
• DROP IN PLASMA OSMOTIC PRESSURE
• INCREASED EXTRACELLULAR FLUID VOLUME
• ALCOHOL
DIABETES INSIPIDUS
• POLYURIA
• POLYDYPSIA
• LOSS OF ADH RELEASE
• IMPAIRED WATER CONSERVATION
• EXCESSIVE WATER LOSS IN URINE
OXYTOCIN
• WOMEN
• MEN
OXYTOCIN IN WOMEN
• STIMULATES SMOOTH MUSCLE IN UTERUS
• PROMOTES LABOR AND DELIVER
• STIMULATES MYOEPITHELIAL CELLS OF MAMMARY GLANDS
OTHER SOURCES OF OXYTOCIN
• FETUS
• UTERUS
NEUROENDOCRINE REFLEXES
CONTROL
OXYTOCIN IN MALES
• UNCERTAIN
• STIMULATES SMOOTH MUSCLE CONTRACTIONS IN DUCTUS DEFERENS AND PROSTATE
OXYTOCIN AND SEX
• AROUSAL AND ORGASM
• EMISSION
• CONTRACTIONS THAT PROMOTE SPERM TRANSPORT
HORMONES OF THE HYPOTHALAMUS &
ADENOHYPOPHYSIS
• ADENOHYPOPHYSEAL HORMONES
• TSH• ACTH• FSH• LH• PRL• GH• MSH• LIPOTROPIN
• RELEASING AND INHIBITING HORMONES FROM THE HYPOTHALAMUS• TRH• CRH• GnRH• GnIH• PRH/PIH• GH-RH/SOMATOSTATIN
THYROID STIMULATING HORMONE
• THYROTROPIN
• RELEASE REGULATED BY THYROTROPIN RELEASING HORMONE (TRH)
• TARGET CELLS IN THYROID
• TRIGGERS RELEASE OF THYROID HORMONE
ADRENOCORTICOTROPIC HORMONE
• DERIVED FROM PROOPIMELANOCORTIN
• INCREASES SECRETION OF ADRENAL HORMONES
• BINDS TO MELANOCYTES AND INCREASE PIGMENTATION OF SKIN
OTHER SUBSTANCES DERIVED FROM PROOPIMELANOCORTIN
• LIPOTROPINS
• BETA ENDORPHINS
• MELANOCYTE STIMULATING HORMONE
LIPOTROPINS
• SECRETED FROM SAME CELLS AS ACTH
• BIND TO MEMBRANE RECEPTORS OF ADIPOSE CELLS
• CAUSE FAT BREAKDOWN & RELEASE OF FATTY ACIDS INTO CIRCULATION
BETA ENDORPHINS
• SAME EFFECT AS OPIATES
• IMPORTANT FOR ANALGESIA IN RESPONSE TO STRESS AND EXERCISE
• MAY BE INVOLVED INBODY TEMPERATUREFOOD INTAKEWATER BALANCE
• STRESS INCREASES SECRETION ALONG WITH ACTH
MELANOCYTE STIMULATING HORMONE
• BINDS TO MELANOCYTES
• STIMULATES DEPOSITION OF MELANIN
• NOT WELL UNDERSTOOD IN HUMANS
• IMPORTANT REGULATOR IN OTHER VERTEBRATES
• PRODUCED IN PARS INTERMEDIAIN HUMANS PARS INTERMEDIA MERGES WITH PARS DISTALIS
RELATIONSHIP BETWEEN MELANOCYTE STIMULATING
HORMONE AND ACTH
• MSH IS SECRETED ALONG WITH ACTH
• USUALLY NOT IN QUANTITIES LARGE ENOUGH TO HAVE A SIGNIFICANT EFFECT
• MAY BE SIGNIFICANT IN ADDISON’S DISEASE
GONADOTROPINS
GONADOTROPINS
• HORMONES PROMOTE GROWTH AND FUNCTION OF GONADS
• LUTEINIZING HORMONE
• FOLLICLE STIMULATING HORMONE
PROLACTIN IN FEMALES
• STIMULATES THE DEVELOPMENT OF DUCT SYSTEM IN MAMMARY GLANDS
WITH OTHER HORMONES• STIMULATES MILK PRODUCTION• USUALLY INHIBITED BY PROLACTIN
INHIBITING HORMONE• STIMULATED BY PROLACTIN
RELEASING HORMONE
PROLACTIN IN MALES
• MAKES INTERSTITIAL CELLS MORE RESPONSIVE TO LUTEINIZING HORMONE
GROWTH HORMONE
• SECRETION STIMULATED BY GROWTH HORMONE RELEASING HORMONE
• SECRETION INHIBITED BY GROWTH HORMONE INHIBITING HORMONE/SOMATOSTATIN
GROWTH HORMONE
• STIMULATES GROWTH OF CARTILAGE AND BONE
• INDIRECT EFFECTS
• DIRECT EFFECTS
INDIRECT EFFECTS
• SOMATOMEDINS /INSULIN-LIKE GROWTH FACTORS
• PEPTIDE HORMONES
• BIND TO MEMBRANE RECEPTORS
• SKELETAL MUSCLE, CARTILAGE AND OTHER TARGET CELLS
DIRECT EFFECTS
• STIMULATES STEM CELL DIVISION AND GROWTH OF DAUGHTER CELLS
EFFECTS OF GROWTH HORMONE ON METABOLISM
• INCREASED PROTEIN SYTHESIS• INCREASED MOBILIZATION OF
FATTY ACIDS FROM ADIPOSE TISSUE• INCREASED USE OF FATTY ACIDS
FOR ENERGY• DECREASED USE OF GLUCOSE
THROUGHOUT BODY• SPARING GLUCOSE FOR THE BRAIN
EFFECTS OF GROWTH HORMONE ON PROTEIN SYNTHESIS
• AMINO ACID TRANSPORT AT THE CELL
• PROTEIN SYNTHESIS BY RIBOSOMES
• INCREASED LEVELS OF RNA
• DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS
AMINO ACID TRANSPORT AT THE CELL
• ENHANCES TRANPORT OF AMINO ACIDS
• WORKS WITH INSULIN
• INCREASED AMINO ACID LEVELS LEAD TO INCREASED PROTEIN SYNTHESIS
PROTEIN SYNTHESIS BY RIBOSOMES
• DIRECT EFFECT ON RIBOSOMES
INCREASED LEVELS OF RNA
• INCREASES TRANSCRIPTION RATE
• OVER TIME INCREASES LEVELS OF RNA
• INCREASED RNA MEANS INCREASED PROTEIN SYNTHESIS
DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS
• DECREASE IN BREAKDOWN OF PROTEINS TO AMINO ACIDS
• DECREASE OF USE OF AMINO ACIDS FOR ENERGY SOURCE
• MAY BE DUE TO MOBILIZATION OF FATTY ACIDS SPARING PROTEIN
EFFECTS OF GROWTH HORMONE ON FAT METABOLISM
• CAUSE LIPOLYSIS AND THE RELEASE OF FATTY ACIDS INTO BODY FLUIDS AND CIRUCLATION
• ENHANCES CONVERSION OF FATTY ACIDS TO ACETYL CO A
• INCREASES USE OF ACETYL CO A FOR ENERGY
• FAT METABOLISM FAVORED OVER CARBOHYDRATE AND PROTEIN METABOLISM
GROWTH HORMONE STIMULATES FATTY ACID
METABOLISMSPARES GLUCOSE AND AMINO
ACIDS
EFFECTS OF GROWTH HORMONE ON CARBOHYDRATE
METABOLISM• DECREASES USE OF GLUCOSE FOR
ENERGY
• ENHANCES GLYGOGENESIS
• DIMINISHES GLUCOSE UPTAKE BY CELLS
DECREASED USE OF GLUCOSE FOR ENERGY
• PERHAPS DUE TO INCREASED MOBILIZATION AND UTILIZATION OF FATS
ENHANCES GLYCOGENOGENESIS
• GLUCOSE WILL BE STORED AS GLYCOGEN
• RESERVES RAPIDLY FILL UP
DIMINISHED GLUCOSE UPTAKE BY CELLS
• INITIAL INCREASED GLUCOSE UPTAKE
• UNTIL GLYCOGEN RESERVE IS FILLED
• THEN UPTAKE DIMINISHES
• GREATLY INCREASED BLOOD GLUCOSE LEVELS
SECRETION OF GROWTH HORMONE
• 3 NANOGRAMS IN ADULT
• 5 NANOGRAMS IN CHILD
• REGULATED BY GH-RH AND SOMATOSTATIN
FEEDBACK CONTROL OF GROWTH HORMONE SECRETION
HORMONES OF THE THYROID GLAND
THYROID HORMONE AND CALCITONIN
THYROID HORMONE
• THYROXINE (T4 )
• TRIIODOTHRYONINE (T3 )
IMPORTANCE OF THYROGLOBULIN
• GLYCOPROTEIN
• CONTAINS 140 TYROSINE AMINO ACIDS
• SUBSTRATE IODINE BINDS WITH
• HORMONES FORM WITHIN THYROGLOBULIN MOLECULE
IMPORTANCE OF IODINE
• USED ONLY TO MAKE THYROID HORMONES
• STORED IN THYROID
• IDODIDE PUMP TRAPS IODIDE
THE WEDDING OF THYROGLOBULIN AND IODIDE
IONS
• OCCURS AT THE COLLOID-CELL INTERFACE AS THYROGLOBULIN IS SECRETED
MIT AND DIT
• MONOIODTYROSINE
• DIIODOTYROSINE
• THYROXINE
• TRIIODOTHRYRONINE
THYROGLOBULIN STORAGE
• IN COLLOID OF FOLLICLE
• ONLY HORMONE STORED EXTRACELLULARLY
• 1-3 MONTH SUPPLY IN COLLOID
RELEASE OF THYROID HORMONE INTO THE
BLOOD• THYROGLOBULIN IS PICKED UP BY
FOLLICULAR CELLS
• LYSOSOMES FUSE WITH PINOCYTIC VESICLES
• THYROXINE AND TRIIODOTHYRONINE ARE CLEAVED FROM THRYOGLOBULIN AND RELEASED
TRANSPORT IN THE BLOOD
• THRYOXINE BINDING GLOBULIN
• ALBUMINS
THYROID HORMONES AT THE CELLS
• ENTERS CELLS
• BINDS WITH INTRACELLULAR PROTEIN RECEPTOR
• THYROXINE HAS GREATER AFFINITY
IMPORTANCE OF LATENCY AND DURATION OF ACTION
• T4 -- TWO OR THREE DAY LATENT PERIOD
• MAXIMUM ACTIVITY IN 10-12 DAYS
• T3 --- 6 TO 12 HOURS
• MAXIMUM ACTIVITY IN 2-3 DAYS
MAJOR EFFECTS OF THYROID HOROMONE
• GROWTH IN CHILDREN
• INCREASE IN METABOLIC RATE
EFFECTS ON GROWTH
• LACK OF THRYOID HORMONE RETARDS GROWTH
• EXCESS OF THYROID HORMONE ENHANCES GROWTH IN CHILD
• CAUSES EPIPHYSEAL PLATES TO CLOSE PREMATURELY SO FINAL HEIGHT MAY BE SHORTENNED
GENERALIZED EFFECTS ON METABOLISM
• AFFECT METABOLISM OF ALMOST ALL CELLS OF BODY
• CALORIGENIC EFFECT
EFFECT OF THYROID HORMONE ON PROTEIN SYNTHESIS
• PHASE ONE--INCREASED TRANSLATION
• PHASE TWO--INCREASED TRANSCRIPTION
EFFECT OF THYROID HORMONE ON CELLULAR
ENZYME SYSTEMS
• INCREASED PROTEIN SYNTHEIS RESULTS IN INCREASED CELLULAR ENZYMES
• AS MUCH AS 6 TIMES NORMAL
EFFECTS ON CELLULAR ORGANELLES
• INCREASED ACTIVITY OF MITOCHONDRIA
• INCREASED NUMBER OF MITOCHONDRIA
EFFECTS ON ACTIVE TRANSPORT
• Na-K ATPase PUMPS INCREASE
• INCREAED TRANSPORT OF SODIUM AND POTASSIUM
EFFECTS ON CARBOHYDRATE METABOLISM
• RAPID UPTAKE OF GLUCOSE
• INCREASED GLYCOLYSIS
• INCREASED GLUCONEOGENESIS
• INCREASED GI ABSORPTION
• INCREASED INSULIN SECRETION
EFFECT ON FAT METABOLISM
• LIPOGENESIS
• LIPOLYSIS
• MOBILIZATION OF LIPIDS
EFFECTS ON BODY MASS
• INCREASED THYROID HORMONE DECREASES
• DECREASED THYROID HORMONE INCREASES
EFFECTS ON CARDIOVASCULAR SYSTEM
• INCREASED OXYGEN DEMAND
• INCREASED METABOLIC WASTE PRODUCTS
• CAUSE VASODILATION
• NEED FOR HEAT ELIMINATION ALSO CAUSES VASODILATION
• CARDIAC OUTPUT CAN INCREASE BY 50%
EFFECTS ON RESPIRATION
• INCREASED OXYGEN DEMAND
• INCREASED CARBON DIOXIDE LEVELS
• ACTIVATE MECHANISMS THAT INCREASE THE RATE AND DEPTH OF RESPIRATION
EFFECT ON GASTROINTESTINAL TRACT
• INCREASE ABSORPTION RATE
• INCREASES SECRETION OF DIGESTION JUICES
• INCREASES MOTILITY OF GASTROINTESTINAL TRACT
• TO MUCH MAY LEAD TO DIARRHEA
• TO LITTLE CONSTIPATION
EFFECT ON THE CENTRAL NERVOUS SYSTEM
• NORMAL AMOUNTS INCREASE CEREBRATION
• TO LITTLE DECREASES CEREBRATION
• TO MUCH -- EXTREME NERVOUSNESS, PSYCHONEUROTIC TENDENCIES, MUSLE TREMOR, TIREDNESS BUT INABILITY TO SLEEP
• TO LITTLE -- MENTAL SLUGGISHNESS EXTREME SOMNOLENCE
SECRETION OF THYROID HORMONE
• TSH FROM ADENOHYPOPHYSIS STIMULATES ITS SECRTION
TRH STIMULATES TSH SECRETION
NEGATIVE FEEDBACK CONTROLS OF THYROID
HORMONE RELEASE
• LONG FEED BACK LOOPS
• SHORT FEEDBACK LOOPS
LONG FEEDBACK LOOP
• INHIBITORY EFFECTS OF TARGET ORGANS ON ADENOHYPOPHYSIS
• THYROID HORMONES COULD ACT ON HYPOTHALAMUS AND INHIBIT SECRETION OF TRH
• THYROID HORMONE COULD ACT ON ADENOHYPOPHYSIS AND INHIBIT ITS RESPONSE TO RELEASING HORMONES
SHORT FEEDBACK LOOPS
• PITUITARY HORMONES THEMSELVES INFLUENCE SECRETION OF RELEASING OR INHIBITING HORMONES
THYROID STIMULATING HORMONE
• HIGH SECRETION OF TSH MAY INHIBIT SECRETION OF TRH
SPECIFIC EFFECTS OF TSH
• INCREASED PROTEOLYTIC ACTIVITY IN FOLLICLES• INCREASED RELEASE OF THYROID HORMONE INTO
BLOOD STREAM• INCREASED TRAPPING OF IODIDE IONS• INCREASED IODINATION OF TYROSINE• INCREAS`E IN SIZE AND ACTIVITY OF FOLLICULAR
CELLS• INCREASED NUMBER OF FOLLICULAR CELLS
REGULATION OF THRYOID HORMONE SECRETION
• TSH FROM PITUITARY STIMULATES SYNTHESIS AND RELEASE
• TRH PROMOTES TSH RELEASE
• NEGATIVE FEED BACK
CALCITONIN
• POLYPEPTIDE
• PRODUCED BY PARAFOLLICULAR CELLS
• LOWERS BLOOD CALCIUM AND PHOSPHATE LEVELS
• SUPRESSES BONE RESORPTION
• INCREASES BONE FORMATION
• IMPORTANT IN BONE REMODELING
HOW CALCITONIN REDUCES BLOOD CALCIUM LEVELS
• DECREASES OSTEOLYTIC EFFECT FAVORS DEPOSITION RATHER THAN RESORPTION
• INCREASES ACTIVITY OF OSTEOBLASTS
• PREVENTS FORMATION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS
CHILDREN VS ADULTS
• MAJOR ROLE IN CHILD
• MINOR ROLE IN ADULTS
REGULATION OF CALCITONIN SECRETION
• 10% RISE IN PLASMA CALCIUM LEVELS LEADS TO 3-6 TIMES MORE CALCITONIN
OTHER IMPORTANT EFFECTS OF CALCITONIN
• REDUCES LOSS OF BONE MASS DURING
PROLONGED STARVATIONLATE STAGES OF PREGNANCY
DIFFERENCES BETWEEN CALCITONIN AND
PARATHYROID HORMONE
• CALCITONIN MORE RAPID
• SHORT TERM REGULATOR
REGULATION OF SECRETION
• PLASMA LEVELS OF CALCIUM
• HIGH CONCENTRATION -- INCREASED SECRETION
• LOW CONCENTRATION -- DECREASED SECRETION
• GASTRIN AND OTHER INTESTINAL HORMONES EFFECT SECRETION
PARATHYROID GLAND
• SMALL FLATTENED GLANDS
• POSTERIOR SURFACE OF THYROID GLAND
CELLS OF PARATHYROID
• CHIEF CELLS
• OXYPHIL CELLS
PARATHYROID HORMONE
• PTH
• POLYPEPTIDE
• TWO OR THREE FORMS
• PRINCIPAL CONTOLLER OF CALCIUM AND PHOSPHATE IN BLOOD
• INCREASES PLASMA CONCENTRATION OF CALCIUM
• DECREASES PLASMA CONCENTRATION OF PHOSPHORUS
ORGANS AFFECTED BY PARATHYROID HORMONE
• BONES
• KIDNEY
PTH EFFECTS ON BONE
• OSTEOLYTIC EFFECT (BONE RESORPTION)
• PROLIFERATION OF OSTEOCLASTS
PTH EFFECT ON OSTEOCLASTS
• IMMEDIATE ACTIVATION OF OSTEOCLASTS
• PRODUCTION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS
EFFECT OF PTH ON THE KIDNEYS
• EXCRETION AND REABSORPTION
• ACTIVATION OF VITAMIN D
EXRETION AND REABSORPTION
• IMMEDIATE AND RAPID LOSS OF PHOSPHATE IN KIDNEYS
DUE TO DECREASED REABSORPTION OF
PHOSPHATES
• INCREASED REABSORPTION OF CALCIUM IN KIDNEYS
ACTIVATION OF VITAMIN D
• CALCITRIOL
• IMPORTANT FOR DEPOSITION IN BONES
PROMOTES CALCIFICATION
• IMPORTANT FOR ABSORPTION OF CALCIUM IN GI TRACT
REGULATION OF PARATHYROID HORMONE RELEASE
THYMUS
• LOCATED UNDER MEDIASTINUM
• RELATIVELY LARGE IN CHILDREN
• REACHES GREATEST SIZE IN PUBERTY -- 40 g
• BEGINS TO INVOLUTE ON ITSELF AFTER PUBERTY TO 12 g AT 50
• ACCELERATED BY GLUCOCORTICOIDS AND SEX HORMONES
THYMIC HORMONES
• THYMOSIN ALPHA
• THYMOSIN BETA
• THYMOSIN V
• THYMOPOIETIN
• THYMULIN
• AND SOME OTHERS
OTHER SITES OF THYMOSIN SYNTHESIS
• MACROPHAGES
EFFECTS OF THYMOSIN
• DEVELOPMENT OF B AND T LYMPHOCYTES
• INFLUENCES HORMONES OF REPRODUCTIVE SYSTEM
HORMONES OF THE ADRENAL GLAND
CORTICAL VS MEDULLARY HORMONES
HORMONES OF THE ADRENAL MEDULLA
• EPINEPHRINE
• NOREPINEPHRINE
• SIMILAR TO SYMPATHETIC GANGLION
• INNERVATED BY PREGANGLIONIC NERVE FIBERS FROM THE SYMPATHETIC NERVOUS SYSTEM
HORMONE SECRETION
• EPINEPHRINE MAKES UP 75-80 % OF SECRETION
• NOREPINEPHRINE MAKES UP 20-25 % OF SECRETION
• METABOLIC CHANGES REACH PEAK AT ABOUT 30 SECONDS AFTER HORMONE RELEASE
• EFFECTS MAY LAST AS LONG AS SEVERAL MINUTES
ANDRENERGIC RECEPTORS
• ALPHA
• BETA
• ALL ARE G LINKED RECEPTORS
• NON CHANNEL LINKED RECEPTORS
NOREPINEPHRINE
• BINDS WITH– ALPHA 1-- EFFECTIVELY– ALPHA 2 -- EFFECTIVELY– BETA 1-- EFFECTIVELY– BETA 2 --WEAKLY IF AT ALL
EPINEPHRINE
• BINDS EFFECTIVELY WITH– ALPHA 1-- EFFECTIVELY– ALPHA 2 -- EFFECTIVELY– BETA 1-- EFFECTIVELY– BETA 2 --EFFECTIVELY
ALPHA RECEPTORS
• MOST COMMON ALPHA RECEPTOR
• ACTIVATES Gp PROTEINS
• G PROTEINS ACTIVATE ENZYMES
ALPHA 2 RECEPTORS
• LESS COMMON THAN ALPHA 1
• ACTIVATES INHIBITORY GI PROTEINS
• REDUCE THE FORMATION OF cyclic AMP
ALPHA RECEPTORS
• VASOCONSTRICTION• IRIS DILATION• INTESTINAL RELAXATION• INTESTINAL SPHINCTER
CONTRACTION• PILOMOTOR CONTRACTION• BLADDER SPHINCTER CONTRACTION
BETA 1 RECEPTORS
• HEART AND KIDNEYS
• ACTIVATES G PROTEINS
• STIMULATES PRODUCTION OF cyclic AMP
BETA 2 RECEPTOR
• ACTIVATES STIMULATORY G PROTEINS
BETA RECEPTORS• VASODILATION• CARDIOACCELERATION• INCREASED MYOCARDIAL STRENGTH• INTESTINAL RELAXATION• UTERUS RELAXATION• BRONCHIOLE DILATION• CALORIGENESIS• GLYCOGENOLYSIS• LIPOLYSIS• BLADDER RELAXATION
IMPORTANCE OF DIFFERENT RECEPTORS
• AT LEAST PARTIALLY RESPONSIBLE FOR DIFFENCE IN ACTIVITY OF EPINEPHRINE AND NOREPINEPHRINE
GENERALIZED EFFECTS OF EPINEPHRINE AND NOREPINEPHRINE
• MOBILIZATION OF GLYCOGEN
• INCREASES CATABOLISM OF GLUCOSE
• RESERVES IN SKELETAL MUSCLE AND LIVER
• LIPOLYSIS AND MOBILIZATION OF FAT RESERVES
• INCREASE IN RATE AND FORCE OF CARDIAC MUSCLE CONTRACTION
SOME SPECIFIC EFFECTS OF CATECHOLAMINES
VASOCONSTRICTION DUE TO CATECHOLAMINE HORMONES
• VASOCONSTRICTOR MECHANISM
• WORKS WITH SYMPATHETIC NERVOUS SYSTEM
• CONSTRICT MOST BLOOD VESSELS
• CONSTRICT VEINS
• REACH AREAS SYMPATHETIC NERVOUS SYSTEM DOES NOT
VASODILATION BY EPINEPHRINE
• CAUSES MILD VASODILATION
• IN SKELETAL
• IN CARDIAC
DILATION OF BRONCHIOLES BY CATECHOLAMINE HORMONES
• SECRETED IN RESPONSE TO SYMPATHETIC INNERVATION
• RELAX BRONCHIOLES
EFFECT OF EPINEPHRNE ON GLYCOGENOLYSIS
• INNERVATION
• ACTIVATES PHOSPHORYLASE
• IN LIVER AND IN MUSCLES
• BREAKS DOWN GLYCOGEN TO GLUCOSE
EFFECTS OF CATECHOLAMINE HORMONES ON CARDIAC
MUSCLE• INCREASE RATE OF SINOATRIAL
NODE DISCHARGE
• INCREASES RATE OF CONDUCTION
• INCREASES EXCITABILITY OF HEART MUSCLE
• INCREASES PERMEABILITY TO CALCIUM AND SODIUM
EFFECTS OF CATECHOLAMINE HORMONES ON FAT UTILIZATION
• HEAVY EXERCISE BRINGS ABOUT DRAMATIC INCREASE IN FAT UTILILZATION
• DUE TO RAPID RELEASE OF NOREPINEPHRINE AND EPINEPHRINE
• DUE TO SYMPATHETIC INNERVATION OF ADRENAL MEDULLA
• ACTIVATE HORMONE-SENSITIVE LIPASE
• LYPOLYSIS AND MOBILIZATION OF FATTY ACIDS
EFFECTS OF CATECHOLAMINE HORMONES ON SMOOTH MUSCLE
• MOST HORMONES AFFECT SMOOTH MUSCLE
• VARYING DEGREES
• EFFECT WILL DEPEND ON TYPE OF RECEPTOR (INHIBITORY VS EXCITATORY)
THE RELATIONSHIP BETWEEN MEDULLARY
HORMONES AND THE ANS• ACTIVATION OF THE SYMPATHETIC
NERVOUS SYSTEM USUALLY LEADS TO RELEASE OF CATECHOLAMINES BY ADRENAL MEDULLA
• SYMPATHETIC NERVOUS SYSTEM AND ADRENAL MEDULLA SUPPORT ONE ANOTHER
HORMONES OF THE ADRENAL CORTEX
MINERALOCORTICOIDS, GLUCOCORTICOIDS, &
ANDROGENIC HORMONES
ALL ADRENOCORTICOIDS ARE STEROIDS
ALDOSTERONE
• VERY POTENT
• 95% OF MINERALOCORTICOID SECRETION
• PRODUCED BY ZONA GLOMERULOSA
GENERALIZED EFFECTS OF ALDOSTERONE SECRETION
• STIMULATES CONSERVATION OF SODIUM IONS
• STIMULATES ELIMINATION OF POTASSIUM IONS
• REABSORPTION OF SODIUM IONS HAS SECODARY EFFECT OF ENHANCING OSMOTIC REABSORPTION
• INCREASES SENSITIVITY OF TASTE BUDS IN TONGUE TO SALT
TARGET CELLS OF ALDOSTERONE
• KIDNEYS
• SWEAT GALNDS
• SALIVARY GLANDS
• PANCREAS
EFFECT OF ALDOSTERONE ON THE KIDNEYS
• MOST IMPORTANT FUNCTION
• CAUSES TRANSPORT OF SODIUM AND POTASSIUM THROUGH RENAL TUBULES
• CAUSES TRANSPORT OF HYDROGEN IONS THROUGH RENAL TUBULES
EFFECT OF ALDOSTERONE ON TUBULAR REABSORPTION OF Na+ AND TUBULAR SECRETION OF K+
• TUBULAR EPITHELIAL CELLS
• EXCHANGE TRANSPORT
• DISTAL TUBULES AND COLLECTING TUBULES
• CONSERVES Na+ --ELIMINATES K+
EFFECTS OF HIGH CONCENTRATIONS OF ALDOSTERONE
• DECREASE SODIUM LOSS TO A FEW MILLIGRAMS PER DAY
• GREAT INCREASE IN POTASSIUM LOSS IN URINE
EFFECTS OF TOTAL LACK OF ALDOSTERONE
• CAN INCREASE SODIUM LOSS UP TO 20 GRAMS PER DAY
• POTASSIUM IS CONSERVED AND LITTLE IS LOST
EFFECTS OF HIGH ALDOSTERONE ON EXTRACELLULAR WATER
VOLUME• CAN INCREASE EXTRACELLULAR
FLUID VOLUME
• UP TO 10 TO 20% OVER NORMAL
EFFECTS OF ALDOSTERONE LOSS ON EXTRAFLUID VOLUME
• CAN DECREASE EXTRACELLULAR FLUID VOLUME
• UP TO 20 TO 25% BELOW NORMAL
EFFECTS OF EXESSIVE POTASSIUM LOSS
• CAN CAUSE A SERIOUS DECREASE OF POTASSIUM
• HYPOKALEMIA
EFFECTS OF HYPOKALEMIA
• SEVERE MUSCLE WEAKNESS
• MUSCLE PARALYSIS
• DUE TO EFFECTS ON NERVE AND MUSCLE FIBER MEMBRANES
EFFECTS OF HYPERKALEMIA
• CARDIAC TOXICITY OCCURS WHEN POTASSIUM LEVELS DOUBLE
• SYMPTOMSWEAKNESS OF CONTRACTIONARRHYTHMIA
IF LEVELS RISE FURTHER CAN LEAD TO DEATH
EFFECTS OF ALDOSTERONE ON TUBULAR SECRETION OF
HYDROGEN IONS• ALSO CAUSES HYDROGEN IONS TO BE
EXCHANGED FOR SODIUM IONS– TO LESSER EXTENT
• DECREASES HYDROGEN ION CONCENTRATION IN EXTRACELLULAR FLUID
• NOT STRONG EFFECT
• CAUSES MILD DEGREE OF ALKALOSIS
EFFECTS OF ALDOSTERONE LACK ON THE CIRCULATORY
SYSTEM
• CAN CAUSE A 20-25% DECREASE OF BLOOD VOLUME & EXTRACELLULAR FLUIDS
CAN CAUSE CIRCULATORY SHOCK
• WITHOUT TREATMENT MAY DIE WITH 4-8 DAYS
EFFECT OF HYPERSECRETION OF ALDOSTERONE ON THE CIRCULATORY SYSTEM
• EXTRACELLULAR FLUID VOLUME INCREASES
• BLOOD VOLUME INCREASES
• CARDIAC OUTPUT INCREASES
• TO AS MUCH AS 20 TO 30% ABOVE NORMAL AT FIRST
• COMPENSATORY MECHANISMS RETURN IT DOWN TO 5-10 %
FACTORS THAT AFFECT THE REGULATION OF
ALDOSTERONE SECRETION• POTASSIUM ION CONCENTRATION
OF THE EXTRACELLULAR FLUID
• RENIN-ANGIOTENSIN SYSTEM
• QUANTITY OF BODY SODIUM
• ADENOCORTICOTROPIC HORMONE
ALDOSTERONE IS NOT AS DEPENDENT ON CRH AND
ACTH
ANGIOTENSIN AND POTASSIUM LEVELS ARE THE MAJOR
REGULATORS
IMPORTANCE OF POTASSIUM IONS IN ALDOSTERONE
SECRETION• INCREASE IN POTASSIUM IONS
CAUSES INCREASED SECRETION OF ALDOSTERONE
• ALDOSTERONE CAUSES ENHANCED EXCRETION OF POTASSIUM
• POTASSIUM LEVELS RETURN TO NORMAL
EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON
ALDOSTERONE SECRETION
RENIN
• KEY IN RENIN-ANGIOTENSIN SYSTEM
• RELEASED BY JUXTAGLOMERULAR COMPLEX OF KIDNEYS
• SECRETED AS PRORENIN
• CONVERTED TO RENIN BEFORE ENTERING BLOODSTREAM
FACTORS THAT INCREASE RENIN SECRETION
• SYMPATHETIC INNERVATION
• DECLINE IN RENAL BLOOD FLOW
EFFECTS OF RENIN
• CATALYZES CONVERSION OF ANGIOTENSINOGEN TO ANGIOTENSIN I
• ANGIOTENSIN I CONVERTED TO ANGIOTENSIN II AS PASSES THROUGH LUNGS
• ANGIOTENSIN CONVERTING ENZYME (ACE)
EFFECTS OF ANGIOTENSIN II• STIMULATES SECRETION OF ADH
STIMULATES WATER REABSORPTIONCOMPLEMENTS ALDOSTERONE
• STIMULATES SECRETION OF ALDOSTERONE BY ADRENAL GLANDSINCREASES RETENTION OF SODIUMINCREASES LOSS OF POTASSIUM
• STIMULATES THIRSTINCREASES FLUID CONSUMPTION INCREASES BLOOD VOLUME
• INCREASES CONSTRICTION OF ARTERIOLESELEVATES SYSTEMIC BLOOD PRESSURE
EFFECTS OF ALDOSTERONE AT THE CELLULAR LEVEL
CORTISOL
GENERALIZED EFFECTS OF CORTISOL
• CARBOHYDRATE METABOLISM
• PROTEIN METABOLISM
• FAT METABOLISM
• STRESS MANAGEMENT
• ANTI-INFLAMMATORY EFFECTS
EFFECTS OF CORTISOL ON CARBOHYDRATE
METABOLISM
EFFECT OF CORTISOL ON GLUCONEOGENESIS
• INCREASE 6 TO 10 TIMES
• INCREASES ENZYMES NEEDED TO CONVERT AMINO ACIDS TO GLUCOSE
DUE TO INCREASED TRANSCRIPTION
• INCREASES MOBILILIZATION OF AMINO ACIDS FROM TISSUES
MUSCLE MAIN SOURCE
• INCREASES AMINO ACID CONCENTRATON IN BLOOD
EFFECTS OF CORTISOL ON GLUCOSE UTILIZATION BY CELLS
• MODERATE DECREASE IN GLUCOSE USE
• DECREASE OCCURS SOMEWHERE BETWEEN POINT OF ENTRY AND FINAL DEGRADATION
• COULD ALSO INVOLVE TRANSPORT MECHANISMS
EFFECTS OF CORTISOL ON BLOOD GLUCOSE CONCENTRATIONS
• INCREASED GLUCONEOGENESIS
• DECREASED GLUCOSE USE
• RAISES BLOOD GLUCOSE LEVELS
•
ADRENAL DIABETES
• INCREASE COULD BE AS LARGE AS 50 % ABOVE NORMAL
• SIMILAR TO PITUITARY DIABETES BUT DIFFERENT FROM INSULIN DEFICIENCY
EFFECT OF CORTISOL ON PROTEIN METABOLISM
EFFECTS OF CORTISOL ON CELLULAR PROTEINS STORES
• REDUCES PROTEIN STORESEXCEPT IN LIVER
• DECREASED PROTEIN SYNTHESIS
• DECREASE IN FORMATION OF RNA
• INCREASED CATABOLISM OF PROTEIN
• DECREASED TRANSPORT OF AMINO ACIDS INTO TISSUES OTHER THAN LIVER
EFFECTS OF CORTISOL ON THE LIVER AND PLASMA
PROTEIN CONCENTRATIONS
• SYNTHESIS OF PROTEINS IN LIVER INCREASES– INCREASED ACTIVITY OF LIVER
ENZYMES
• PLASMA PROTEINS PRODUCED ARE RELEASED INTO BLOOD
EFFECTS OF CORTISOL ON MOVEMENTS OF AMINO ACIDS INTO AND OUT OF THE BLOOD
AND BLOOD AMINO ACID CONCENTRATIONS
• DEPRESSES UPTAKE BY MUSCLE AND OTHER CELLS
• INCREASED UPTAKE BY LIVER
• INCREASES PLASMA CONCENTRATIONS OF AMINO ACIDS
EFFECTS OF INCREASED PLASMA CONCENTRATIONS OF AMINO ACIDS ON
LIVER UTILIZATION OF AMINO ACIDS
• INCREASED DEAMINATION OF AMINO ACIDS
• INCREASED PROTEIN SYNTHESIS
• INCREASED SYNTHESIS OF PLASMA PROTEINS
• INCREASED GLUCONEOGENESIS
EFFECTS OF CORTISOL ON FAT METABOLISM
EFFECT OF CORTISOL ON THE MOBILIZATION OF FATS
• INCREASES MOBILIZATION OF FATTY ACIDS FROM ADIPOSE TISSUE
• INCREASES PLASMA FATTY ACID CONCENTRATIONS• MODERATELY INCREASES OXIDATION OF FATTY
ACIDS• SHIFTS BODY TO FAT METABOLISM IN STARVATION
OR STRESS• EFFECT DEVELOPS OVER SEVERAL HOURS• GLYCOGEN AND GLUCOSE SPARER
OTHER EFFECTS OF CORTISOL
EFFECTS OF CORTISOL IN STRESSFUL SITUATION
• ANY KIND OF STRESS INCREASES ACTH SECRETION
• INCREASED SECRETIONS OF CORTISOL
IN MINUTES
EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
• INFLAMMATION IS TRIGGERED BY TRAUMA, INFECTION OR A VARIETY OF OTHER MECHANISMS
• CORTISOL CAN BLOCK INFLAMMATION
• CAN EVEN REVERSE MANY OF ITS EFFECTS
SPECIFIC EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
• STABILIZES LYSOSOMAL MEMBRANES
• BLOCKS MOST OF THE FACTORS CAUSING INFLAMMATION
• INCREASES HEALING PROCESS
IMPORTANCE OF CORTISOL IN FIGHTING DISEASE
• RHEUMATOID ARTHRITIS
• RHEUMATIC FEVER
• ACUTE GLOMERULONEPHRITIS
CONTROL OF CORTISOL SECRETION
• ACTH IS THE MAJOR FACTOR CAUSING CORTISOL SECRETION
EFFECT OF CORTICOTROPIN RELEASING HORMONE IN
ACTH SECRETION
• SMALL PEPTIDE FROM HYPOTHALAMUS
• LITTLE ACTH IS SECRETED IN THE ABSENCE OF CRH
EFFECTS OF PHYSIOLOGICAL STRESS
ON ACTH SECRETION
• CAN LEAD TO INCREASE ACTH
• CAN RESULT IN INCREASED LEVELS OF CORTISOL WITHIN A FEW MINUTES
• REGULATED BY HYPOTHALAMUS AND THE RELEASE OF CRH
FEEDBACK CONTROLS ON ACTH SECRETION
• CORTISOL HAS A DIRECT NEGATIVE FEEDBACK EFFECT – ON HYPOTHALAMUS DECREASING CRH– ON ANTERIOR PITUITARY DECREASING
ACTH
HORMONES OF THE PANCREAS
PANCREATIC HORMONES
• GLUCAGON
• INSULIN
• SOMATOSTATIN
• PANCREATIC POLYPEPTIDE
SOMATOSTATIN
• PRODUCED BY DELTA CELLS
• IDENTICAL TO BRAIN FORM
• SUPPRESSES RELEASE OF GLUCAGON AND INSULIN
• SLOWS RATE OF FOOD ABSORPTION
• SLOWS RATE OF ENZYME SECRETION
PANCREATIC POLYPEPTIDE
• INHIBITS GALLBLADDER CONTRACTIONS
• REGULATES PRODUCTION OF SOME PANCREATIC ENZYMES
• MAY HELP IN CONTOLLING RATE OF ABSORPTION IN GI TRACT
INSULIN
• POLYPEPTIDE HORMONE• SECRETED BY BETA CELLS• WHEN GLUCOSE LEVELS RISE ABOVE
NORMAL LEVELSOR
• WHEN ELEVATED LEVELS OF ARGININE, LEUCINE AND OTHER HORMONES ARE PRESENT IN THE BLOOD
INSULIN DEPENDENT CELLS
• MOST ALL THE CELL IN BODY
INSULIN INDEPENDENT CELLS
• BRAIN
• KIDNEYS
• LINING OF GI TRACT
• RED BLOOD CELLS
GENERALIZED EFFECTS OF INSULIN• ACCELERATION OF GLUCOSE UPTAKE IN ALL TARGET CELLS
• ACCELERATION OF GLUCOSE UTILIZATION IN ALL TARGET CELLS
• ENHANCED ATP PRODUCTION IN ALL TARGET CELLS
• STIMULATION OF GLYCOGENESIS IN SKELETAL AND LIVER CELLS
• STIMULATION OF AMINO ACID ABSORPTION IN ALL TARGET TISSUES
• STIMULATION OF PROTEIN SYNTHESIS IN ALL TARGET TISSUES
• STIMULATION OF LIPOGENESIS IN ALL TARGET TISSUES
INSULIN REDUCES THE BLOOD GLUCOSE LEVEL
INSULIN IS A PROTEIN AND FAT SPARER
SPECIFIC EFFECTS OF INSULIN`
EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM
• RAPID UPTAKE OF GLUCOSE
• STORAGE OF GLUCOSE AS GLYCOGEN
• CATABOLISM OF GLUCOSE
• ESPECIALLY IN ADIPOSE, LIVER AND SKELETAL TISSUES
EFFECTS OF INSULIN ON THE UPTAKE, STORAGE AND USE OF
GLUCOSE BY THE LIVER• MOST OF GLUCOSE ABSORBED
AFTER MEAL IS STORED IN LIVER AS GLYCOGEN
• ACTS AS A RESERVE TO SUPPLY GLUCOSE BETWEEN MEALS
MECHANISMS OF GLUCOSE UPTAKE
• INSULIN INHIBITS PHOSPHORYLASE
• ENHANCES UPTAKE OF GLUCOSE BY HEPATOCYTES– INCREASES ACTIVITY OF GLUCOKINASE
• ENZYME PHOSPHORYLATES GLUCOSE TRAPPING IT INSIDE CELL
• INCREASES ACTIVITY OF ENZYMES PROMOTING GLYCOGENESIS
• NET EFFECT IS TO INCREASE GLYOGEN LEVELS IN LIVER
GLYCOGEN STORAGE IN LIVER
• ABOUT 5-6 PERCENT OF LIVER MASS
• USUALLY 100 GRAMS
OTHER EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM
IN THE LIVER• PROMOTES CONVERSION OF LIVER
GLUCOSE INTO FATTY ACIDS
• FATTY ACIDS ARE THEN TRANSPORTED TO ADIPOSE TISSUES AND DEPOSITED
• INHIBITS GLUCONEOGENESIS– DECREASES ACTIVITIES OF ENZYMES
EFFECTS OF INSULIN ON GLUCOSE METABOLISM IN MUSCLE CELLS
• MUSCLES GENERALLY USE FATTY ACIDS AS THEIR ENERGY SOURCE
• RESTING MEMBRANE IS ALMOST IMPERMEABLE TO GLUCOSE
• UNTIL STIMULATED BY INSULIN
CONDITIONS WHERE MUSCLES USE CONSIDERABLE GLUCOSE
• DURING PERIODS OF HEAVY EXERCISE
• DURING THE FIRST FEW HOURS AFTER A MEAL WHEN INSULIN LEVELS ARE HIGH
EFFECTS OF HEAVY EXERCISE ON MUSCLE CELLS
• DOES NOT REQUIRE LARGE AMOUNTS OF INSULIN
• MEMBRANE PERMEABILITY CHANGES DUE TO CONTRACTILE PROCESS
EFFECTS OF INSULIN
• CAUSES RAPID TRANSPORT OF GLUCOSE INTO THE CELLS
EFFECT OF INSULIN ON THE STORAGE OF GLYCOGEN IN
MUSCLE CELLS• IN RESTING MUSCLES AFTER MEAL
• GLUCOSE IS STORED AS MUSCLE GLYCOGEN
• CONCENTRATION CAN BE AS MUCH AS 1-2 % OF CELL MASS
• CAN BE USED AS ENERGY RESERVE
DIFFERENCES BETWEEN LIVER GLYCOGEN AND
MUSCLE GLYCOGEN• MUSCLE GLYCOGEN CANNOT BE
RECONVERTED TO GLUCOSE AND RELEASED INTO BLOOD STREAM WHILE LIVER CELLS CAN
• MUSCLE CELLS DO NOT HAVE GLUCOSE PHOSPHATASE
• LIVER CELLS HAVE GLUCOSE PHOSPHATASE
MECHANISM BY WHICH INSULIN INCREASES GLUCOSE TRANSPORT IN MUSCLE CELLS• SOME GLUCOSE TRAPPING BY
GLUCOKINASE
• ENHANCES FACILITATED DIFFUSION OF GLUCOSE THROUGH MEMBRANE
• TAKES ONLY A FEW SECONDS
EFFECTS OF GLUCOSE ON THE BRAIN
• INSULIN INDEPENDENT
• PERMEABLE TO GLUCOSE WITH OR WITHOUT INSULIN
• BRAIN DEPENDENT ON GLUCOSE
BLOOD GLUCOSE LEVELS ARE MAINTAINED DUE TO THE
BRAINS NEED FOR GLUCOSE
• BLOOD GLUCOSE LEVELS MUST ALWAYS MAINTAIN A CRITICAL LEVEL
• LEVELS IN A RANGE OF 20-50 mg/100 ml CAUSES HYPOGLYCEMIC SHOCK
SYMPTOMS OF HYPOGLYCEMIC SHOCK
• PROGESSIVE IRRITABILITY
• FAINTING
• CONVULSIONS
• COMA
• DEATH
EFFECT OF INSULIN ON FAT METABOLISM
• MAY NOT BE AS DRAMATIC AS CARBOHYDRATE
• BUT IS MORE IMPORTANT• INSULIN IS A PROTEIN SPARER
• EFFECTS OF INSULIN ARE BEST SEEN WHEN THERE IS A LACK OF INSULIN
EFFECTS OF INSULIN ON EXCESS FAT SYNTHESIS AND STORAGE
• SEVERAL EFFECTS LEAD TO AN INCREASE IN FAT STORAGE
• INCREASE IN GLUCOSE UTILIZATION BY MANY OF BODY’S CELLS
• INSULIN ALSO PROMOTES FATTYACID SYNTHESIS IN LIVER
• INSULIN PROMOTES A SMALL AMOUNT OF FATTY ACID SYNTHESIS IN THE ADIPOSE CELLS
FACTORS THAT LEAD TO AN INCREASE IN FATTY ACID SYNTHESIS IN THE LIVER
• INCREASED TRANSPORT OF GLUCOSE INTO HEPATOCYTES
• EXCESS CITRATE AND ISOCITRATE IONS ARE FORMED BY CITRIC ACID CYCLE
• TRANSPORT OF FATTY ACIDS TO THE ADIPOSE TISSUES
INCREASED TRANSPORT OF GLUCOSE INTO THE LIVER
• PHOSPHORYLATION
• CONVERSION OF GLUCOSE TO PYRUVATE
• CONVERSION OF PYRUVATE TO ACETYL-coA
• SYTHESIS OF FATTY ACIDS FROM ACETYL coA
EXCESS CITRATE AND ISOCITRATE IONS FROM THE
CITRIC ACID CYCLE
• FORMED WHEN EXCESSIVE AMOUNTS OF GLUCOSE ARE BEING USED FOR ENERGY
• DIRECTLY ACTIVATE ACETYL-coA CARBOXYLASE– CATALYZES FIRST STAGE OF FATTY
ACID SYNTHESIS
FATTY ACIDS ARE THEN TRANSPORTED TO THE ADIPOSE
TISSUES• REMOVES THEM AND PREVENTS A
NEGATIVE FEEDBACK EFFECT ON ACETYL-co CARBOXYLASE
EFFECTS OF INSULIN OF FAT STORAGE AT THE ADIPOSE
TISSUES• SAME EFFECT AS IN THE LIVER BUT
SMALLER
• ONE TENTH AS MUCH GLUCOSE IS TRANSPORTED INTO ADIPOSE CELLS
ESSENTIAL EFFECTS OF INSULIN ON FAT STORAGE IN THE ADIPOSE TISSUES
• INHIBITS THE ACTIVITY OF HORMONE SENSITVE LIPASE– CATALYZES LIPOLYSIS
• PROMOTES TRANSPORT OF GLUCOSE INTO CELLS
SAME AS IN MUSCLE CELLSUSED TO FORM GLYCEROL
WHEN INSULIN IS NOT AVAILABLE FAT STORAGE IS GREATLY INHIBITED IF
NOT BLOCKED
EFFECTS OF INSULIN ON PROTEIN METABOLSISM
• WITH GH PROMOTES UPTAKE OF AMINO ACIDS INTO CELLS
• DIRECTLY AFFECTS RIBOSOME TO CAUSE TRANSLATION
• INCREASES (OVER TIME) TRANSCRIPTION
• INHIIBITS CATABOLISM OF PROTEINS
• INHIBITS GLUCONEOGENESIS ENZYMES IN LIVER
INSULIN GREATLY ENHANCES PROTEIN
SYNTHESIS AND DECREASES DEGRADATION
OF PROTEINS
EFFECT OF INSULIN ON GROWTH
• INSULIN WORKS WITH GROWTH HORMONE– SYNERGISTIC EFFECT
• ANIMALS DEPRIVED OF EITHER PITUITARY OR PANCREAS DISPLAY STUNTED GROWTH
• BOTH NEED TO BE PROVIDED FOR NORMAL GROWTH
CONTROL OF INSULIN SECRETION
• BY BLOOD GLUCOSE LEVELS IN THE BLOOD
• BY AMINO ACID LEVELS IN THE BLOOD
• BY GASTROINTESTINAL HORMONES
EFFECTS OF BLOOD GLUCOSE LEVELS ON INSULIN SECRETION
• 80-90 mg/100ML--MINIMAL INSULIN SECRETION
• ABOVE 100mg/100ML --INSULIN SECRETION RISES QUICKLY
• CAN REACH AS MUCH AS 400 - 600 mg/100ML • SECRETION DECREASES RAPIDLY AS
BLOOD GLUCOSE LEVELS RETURN TO FASTING LEVEL
EFFECT OF AMINO ACIDS ON INSULIN SECRETION
• SOME OF THE AMINO ACIDS CAUSE INCREASED SECRETION– IE ARGININE AND LEUCINE
• AMINO ACIDS ADMINISTERED WITHOUT AN ACCOMPANYING RISE IN BLOOD GLUCOSE WILL CAUSE ONLY A SMALL RISE IN SECRETION
• IF BOTH ARE PRESENT INSULIN SECRETION MAY BE DOUBLED
EFFECT OF GASTROINTESTINAL HORMONES ON INSULIN
SECRETION• GASTRIN
• SECRETIN
• CCK
• GASTRIC INHIBITORY PEPTIDE
• RELEASED AFTER EATING
• SEEM TO CAUSE AN ANTICIPITORY RISE IN INSULIN SECRETION
• ALMOST DOUBLE SECRETION OF INSULIN AFTER A MEAL
CARBOHYDRATE VS FATTY ACID (LIPID) METABOLISM
INSULIN DETERMINES WHICH WILL OCCUR
GLUCAGON
• PRODUCED BY ALPHA CELLS
GENERALIZED EFFECTS OF GLUCAGON
• GLYCOGENOLYSIS IN SKELETAL AND LIVER CELLS
• LIPOLYSIS AND FATTY ACID MOBILIZATION IN ADIPOSE TISSUES
• GLUCONEOGENESIS AT THE LIVER
• REDUCTION OF GLUCOSE UTILIZATION
• INCREASE IN BLOOD GLUCOSE LEVELS
GLUCAGON IS A GLUCOSE SPARER
GLYCOGENOLYSIS AND INCREASED BLOOD GLUCOSE
LEVELS CAUSED BY GLUCAGON• MOST DRAMATIC EFFECT
• INCREASES BLOOD GLUCOSE LEVELS IN MINUTES
MECHANISMS OF ACTIVATING GLYCOGENOLYSIS IN THE LIVER
• ACTIVATES ADENYLATE CYCLASE• FORMS c AMP• ACTIVATES PROTEIN KINASE REGULATOR PROTEIN• ACTIVATES PROTEIN KINASE• ACTIVATES PHOSPHORYLASE b KINASE• CONVERTS PHOSPHORYLASE b INTO PHOSPHORYLASE a• PROMOTES THE PHOSPHORLYSIS OF GLYCOGEN INTO
GLUCOSE 1 PHOSPHATE• GLUCOSE 1 PHOSPHATE IS DEPHOSPHORYLATED AND
LEAVES THE HEPATOCYTE BY FACILITATED DIFFUSION
EFFECT OF GLUCAGON ON GLUCONEOGENESIS IN THE LIVER• NONCARBOHYDRATE SUBSTRATES ARE CONVERTED TO
PYRUVATE OR AN INTERMEDIATE IN THE CITRIC ACID CYCLE
• AMINO ACIDS ARE CONVERTED TO PYRUVATE OR PHOSPHOPHENOLPYRUVATE
• LIPIDS CAN BE CONVERTED TO PGA, PGAL OR ANOTHER 3 CARBON INTERMEDIATE
• GLUCONEOGENESIS HAS SAME INTERMEDIATES AS GLYCOLYSIS
• BUT ITS ENZYMES RUN IT FROM PYRUVATE TO GLUCOSE
REGULATION OF GLUCAGON SECRETION
• BLOOD GLUCOSE CONCENTRATIONS• OPPOSITE EFFECT THAN IT HAS ON
INSULIN• WHEN BLOOD GLUCOSE FALLS AS
LOW AS 70mg/100ML LARGE AMOUNTS OF GLUCAGON ARE SECRETED
• PROTECTS THE BODY AGAINST HYPOGLYCEMIA
EFFECTS OF AMINO ACIDS ON GLUCAGON SECRETION
• HELPS PREVENT HYPOGLYCEMIA THAT WOULD OCCUR IF YOU ATE A MEAL OF PURE PROTEIN
IMPORTANCE OF BLOOD GLUCOSE REGULATION
ITS ALL FOR THE BRAIN
IN NORMAL INDIVIDUAL
• BLOOD GLUCOSE LEVELS ARE TIGHTLY REGULATED
• BETWEEN 80-90 IN THE MORNING
• 120 TO 140 AFTER BREAKFAST
• RETURN TO NORMAL IN ABOUT 2 HOURS AFTER MEAL
MAINTENANCE OF BLOOD GLUCOSES BETWEEN MEALS
• LIVER ACTS AS A BLOOD GLUCOSE BUFFER– STORES GLUCOSE AFTER MEALS
• AS MUCH AS 2/3 OF GLUCOSE ABSORBED IS STORED IN LIVER AS GLYCOGEN
– RELEASES GLUCOSE BETWEEN MEAL• INSULIN AND GLUCAGON FUNCTION AS SEPARATE CONTROL SYSTEMS• IN HYPOGLYCEMIA SYMPATHETIC INNERVATION INCREASES AND
STIMULATES RELEASE OF EPINEPHRINE WHICH INCREASES GLUCOSE RELEASE
• OVER HOURS OR DAYS--GH AND CORTISOL ARE RELEASED – DECREASE GLUCOSE UTILIZATION
THEY DO IT ALL FOR THE BRAIN
ALSO THE RETINA, GERMINAL EPITHELIA OF GONADS,
KIDNEYS, AND OTHER INSULIN INDEPENDENT CELLS
PINEAL GLAND
• PEA SIZED
• EPITHALAMUS
• ROOF OF DIENCEPHALON
• NEUROENDOCRINE TRANSDUCER
NEUROENDOCRINE TRANSDUCER
• CONVERTS SIGNALS RECEIVED THROUGH NERVOUS SYSTEM INTO AN ENDOCRINE SIGNAL
RELATIONSHIP TO HYPOTHALAMUS
• INFORMATION ABOUT LIGHT AND DARK CYCLES CARRIED FROM EYES TO HYPOTHALAMUS
• SYMPATHETIC NERVES CARRY ACTION POTENTIALS TO PINEAL GLAND
HORMONES OF THE PINEAL GLAND
• MELATONIN
• OTHERS HAVE BEEN FOUND BUT THEY DO NOT KNOW THEIR FUNCTIONS
ARGININE VASOTOCIN
MELATONIN
• DERIVED FROM SERATONIN
• PRODUCTION LOWEST IN DAYLIGHT
• PRODUCTION HIGHEST AT NIGHT
EFFECTS OF MELATONIN
• SLOWS MATURATION OF SPERM, EGGS AND REPRODUCTIVE ORGANS
REDUCES RATE OF GnRH SECRETION
• EFFECTIVE ANTIOXIDANT
• MAY BE INVOLVED IN CIRCADIAN RHYTHM
• INCREASED SECRETION MAY CAUSE SEASONAL AFFECTIVE DISORDER
HORMONES OF THE REPRODUCTIVE TISSUES
• MALE
• FEMALE
• REGULATED BY FSH AND LH
THE HORMONES OF THE TESTES
• TESTOSTERONE
• INHIBIN
HORMONES OF THE OVARIES
• ESTROGENSESTRADIOL, ESTRIN ESTRONE
• PROGESTINSPROGESTERONE
• INHIBIN
• RELAXIN
HORMONES OF THE PLACENTA
• TEMPORARY ORGAN
• ESTROGEN
• PROGESTERONE
• HUMAN CHORIONIC GONADOTROPIN
HORMONE OF THE UTERUS
• RELAXIN
HORMONES OF PREGNANCY
• HUMAN CHORIONIC GONADOTROPIN
• SECRETION OF PROGESTERONE
• SECRETION OF ESTROGEN
• HUMAN CHORIONIC SOMATOMAMMOTROPIN
HUMAN CHORIONIC GONADOTROPIN
• HAS STRUCTURE SIMILAR TO LUTEINIZING HORMONE
• FIRST SECRETED BY TROPHOBLAST CELLS OF BLASTOCYST– BEFORE IMPLANTATION
• SECRETED BY PLACENTA ONCE ESTABLISHED
DIFFUSES FROM FETAL BLOOD INTO MATERNAL BLOOD
• STIMULATES CORPUS LUTEUM– PREVENTS DEGENERATION– PREVENTS INVOLUTION– CAUSES IT TO ALMOST DOUBLE IN SIZE
• STIMULATES CONTINUED SECRETION OF PROGESTERONE– MAINTAINS ENDOMETRIUM
• LATER IN PREGNANCY STIMULATES SECRETION OF PROGESTERONE AND ESTROGEN
• IMPORTANT IN MAINTAINING PREGNANCY IN FIRST 7-10 WEEKS
PLACENTA TAKES OVER SECRETORY FUNCTION AT SECOND
MONTH
• SECRETES ESTROGEN AND PROGESTERONE
• PLACENTA STOPS SECRETING HUMAN CHORIONIC – CAUSING THE CORPUS LUTEUM TO
DEGENERATE AND INVOLUTE
IMPORTANCE OF HUMAN CHORIONIC GONADOTROPIN
• PREVENTS DEGENERATION OF THE CORPUS LUTEUM
• STIMULATES THE CORPUS LUTEUM TO SECRETE ESTROGEN
• STIMULATES THE CORPUS LUTEUM TO SECRETE PROGESTERONE
• STIMULATES SECRETION OF STEROIDS FROM ADRENAL CORTEX OF FETUS
• STIMULATES FETAL GONADS TO SECRETE • SUPRESSES MATERNAL LYMPHOCYTES REDUCING
REJECTION OF THE FETUS
PROGESTERONE SECRETION BY THE PLACENTA
• BEGINS SECRETION ABOUT THE 6TH WEEK OF PREGNANCY
• THIS TOTALLY REPLACES PROGESTERONE FROM THE CORPUS LUTEUM BY THE 12TH -14TH WEEKS
ROLE OF PLACENTAL PROGESTERONE
• MAINTENANCE OF PREGNANCY• STIMULATES GROWTH OF ENDOMETRIUM• STIMULATES SECRETION OF NUTRIENTS
ENDOMETRIAL GLANDS• INHIBITS CONTRACTION OF THE UTERUS• PREVENTS PREMATURE EXPULSION OF FETUS• WORKS WITH PROLACTIN & OXYTOCIN TO
STIMULATE PREPARATIONS FOR LACTATION IN BREAST
• SERVES AS A PRECURSOR FOR PLACENTAL ESTROGEN
PLACENTAL ESTROGEN
• CORPUS LUTEUM SECRETES ESTROGEN FOR FIRST MONTH
• IN RESPONSE TO HUMAN CHORIONIC GONADOTROPIN
• AFTER 1ST MONTH HUMAN CHORIONIC GONADOTROPIN STIMULATES ESTROGEN SECRETION FROM PLACENTA
• LEVELS INCREASE UNTIL DELIVERY
ESTROGEN FUNCTIONS
• STIMULATES ENLARGEMENT OF THE UTERUS
• STIMULATES BREAST GROWTH• STIMULATES DEVELOPMENT OF DUCTS IN
BREAST• STIMULATES ENLARGEMENT OF
GENITILIA• STIMULATES RELAXATION OF PELVIC
LIGAMENTS
IMPORTANCE OF THE FETUS IN SECRETING PLACENTAL ESTROGEN
• PLACENTA LACKS ENZYME IN ESTROGEN PATHWAY
• FETAL ADRENAL CORTEX CONTAINS THE ENZYME NECESSARY TO CONVERT PREGNELONE TO DHEA
• TRANSPORTED BACK TO PLACENTA AND IS CONVERTED INTO ESTRODIOL AND RELEASED
HUMAN CHORIONIC SOMATOMAMMOTROPIN
• SECRETION BEGINS AT ABOUT 4TH WEEK• RISES THROUGHOUT PREGNANCY• SIMILAR TO HUMAN GROWTH HORMONE• WEAKLY STIMULATES FETAL DEVELOPMENT AND
BREAST DEVELOPMENT• ANTAGONISTIC TO INSULIN
– DECREASING MATERNAL USE OF GLUCOSE
– MAKES MORE GLUCOSE AVAILABLE TO FETUS
– CAN CAUSE GESTATIONAL DIABETES IN MOTHER
– PROMOTES MOBILIZATION OF FATS
HORMONAL CHANGES IN PREGNANCY
• INHIBITION OF GONADOTROPIN• STIMULATION OF PROLACTIN• STIMULATION OFRELAXIN• STIMULATION OF INSULIN• STIMULATION OF ALDOSTERONE• STIMULATION OF CORTISOL• STIMULATION OF THYROID HORMONE
INHIBITION OF GONADOTROPINS
• HIGH LEVELS OF ESTROGEN AND PROGESTERONE IN BLOOD STREAM INHIBIT SECRETION OF GONADOTROPIN RELEASING HORMONE
• THIS INHIBITS THE RELEASE OF FOLLICLE STIMULATING HORMONE AND LUTEINIZING HORMONE
• THIS PREVENTS OVULATON AND/OR MENSTRUATION
STIMULATION OF PROLACTIN
• SECRETION INCREASES THROUGHOUT PREGNANCY
• WORKS WITH ESTROGEN AND PROGESTERONE TO STIMULATE BREAST DEVELOPMENT AND MILK PRODUCTION
STIMULATION OF RELAXIN
• HUMAN CHORIONIC GONADOTROPIN STIMULATES RELAXIN SECRETION BY CORPUS LUTEUM IN FIRST TWO MONTHS
• LATER RELAXIN IS SECRETED BY THE ENDOMETRIUM
FUNCTION OF RELAXIN
• RELAXES PELVIC LIGAMENTS
• WORKS WITH PROGESTERONE TO INHIBIT UTERINE CONTRACTIONS
STIMULATION OF INSULIN
• DECREASED MATERNAL SENSITIVITY TO INSULIN CAUSES ITS SECRETION TO INCREASE– AFTER 3RD MONTH
• CAN BECOME SEVERE ENOUGH TO CAUSE GESTATIONAL DIABETES
• NORMALLY RETURNS TO NORMAL AFTER BIRTH
STIMULATION OF ALDOSTERONE
• ESTROGEN AND PROGESTERONE DIRECTLY INCREASE THE SECRETION OF ANGIOTENSIN II AND ALDOSTERONE FROM ADRENAL CORTEX– PROMOTE SODIUM AND WATER RETENTION
– HELPS TO PROVIDE SODIUM TO FETUS
– ESTROGEN SEEMS TO INHIBIT THE VASCULAR EFFECTS OF HIGH LEVELS OF ANGIOTENSIN II
STIMULATION OF CORTISOL
• INCREASES IN CORTISOL SECRETION AND SECRETION OF CORTISOL BINDING GLOBULIN – IN RESPONSE TO STIMULATION OF
ESTROGEN– LEAD TO AN INCREASE IN BOTH FREE
AND PROTEIN BOUND CORTISOL
EFFECTS OF INCREASED CORTISOL LEVELS
• INCREASED BODY FAT• DEVELOPMENT OF MAMMARY GLANDS• INCREASED APPETITE • INCREASED BLOOD GLUCOSE LEVELS• INCREASED GLUCOSE LEVELS INCREASE
INSULIN SECRETION• INCREASED INSULIN SECRETION
INCREASES LIPID STORAGE
INCREASED THYROID HORMONE
• HIGH LEVELS OF ESTROGEN STIMULATE THYROTROPIN RELEASING HORMONE
• STIMULATES THYROID STIMULATING HORMONE
• RESULTS IN INCREASE IN GLAND SIZE, SECRETORY RATE, BASAL METABOLIC RATE, CARDIAC AND PULMONARY FUNCTION
THE ENDOCRINE FUNCTION OF THE HEART
• ATRIOPEPTIN/ATRIAL NATRIURETIC PEPTIDE
• PRODUCED BY ATRIA CARDIAC MUSCLES
EFFECTS OF ATRIAL NATRIURETIC PEPTIDE
• PROMOTES LOSS OF SODIUM IONS AND WATER AT KIDNEYS
• INHIBITS RENIN RELEASE
• INHIBITS SECRETION OF ADH AND ALDOSTERONE
• SUPPRESSES THIRST
• BLOCKS ACTION OF ANGIOTENSIN II AND NOREPINEPHRINE ON ARTERIOLES
ENDOCRINE FUNCTION OF THE DIGESTIVE SYSTEM
HORMONES OF THE DIGESTIVE SYSTEM
• GASTRIN
• SECRETIN
• CHOLECYSTOKININ
GASTRIN
• POLYPEPTIDE
• SECRETED BY MUCOSAL LINING
• STIMULATES PRODUCTION OF HCL AND PEPSIN
SECRETIN
• POLYPEPTIDE
• FIRST HORMONE
• SECRETED BY THE MUCOSA OF THE DUODENUM
• STIMULATES A BICARBONATE RICH SECRETION FROM THE PANCREAS
• CAN INHIBIT GASTRIC SECRETIONS UNDER CERTAIN CONDITIONS
• STIMULATES SECRETION OF BILE
CHOLECYSTOKININ
• SECRETED BY WALL OF DUODENUM
• STIMULATES CONTRACTION OF DUODENUM
• INHIBITS GASTRIC ACID SECRETIONS UNDER CERTAIN CONDITIONS
• STIMULATES THE RELEASE OF ENZYMES FROM THE PANCREAS
HORMONES OF THE KIDNEYS
CALCITRIOL
• STEROID HORMONE
• SECRETED IN RESPONSE TO PTH
• DEPENDENT ON CHOLECALCIFEROLFROM SKIN OR DIETCARRIED BY TRANSCALCIFERIN
• VITAMIN D REFERS TO ALL FORMS OF THE VITAMINS
EFFECT OF CALCITRIOL
• STIMULATION OF CALCIUM AND PHOSPHATE ABSORPTION BY GI TRACT
• STIMULATE FORMATION AND DIFFERENTIATION OF OSTEOPROGENITOR CELLS AND OSTEOCLASTS
• STIMULATING CALCUM REABSORPTION AT THE KIDNEYS
• SUPPRESSES PARATHYROID HORMONE SECRETION
ERYTHROPOIETIN
• PEPTIDE HORMONE
• RELEASED BY KIDNEY IN RESPONSE TO HYPOXIA IN KIDNEY TISSUES
POSSIBLE CAUSES OF HYPOXIA
• REDUCTION IN RENAL BLOOD FLOW
• REDUCTION IN NUMBER OF RED BLOOD CELLS
• REDUCTION IN ABILITY OF RED BLOOD CELLS TO CARRY OXYGEN
• REDUCTION IN OXYGEN CONTENT OF AIR
• PROBLEMS WITH THE RESPIRATORY MEMBRANE
EFFECT OF ERYTHROPOIETIN
• STIMULATES HEMATOPOIESIS
• ELEVATES BLOOD VOLUME SLIGHTLY DUE TO INCREASE IN RED BLOOD CELLS
• IMPROVES OXYGEN DELIVERY TO PERIPHERAL TISSUES
LEPTIN
A NEW HORMONE
EFFECTS OF AGING
• FEW FUNCTIONAL CHANGES
• DECLINE IN LEVELS OF REPRODUCTIVE HORMONES
• ENDOCRINE TISSUES MAY BECOME LESS RESPONSIVE
• SOME TARGET CELLS IN TISSUES MAY BECOME LESS RESPONSIVE