By Ronald Ombaka Esq.

Why regulate?

Agents of regulation

Crucial centers for regulation

Intergration of regulation with practice

Objectives

Why do we need a CVS……….

To deliver and remove metabolic substrates and wastes from; points of entry; to points of use; to points of excretion/elimination, respectively.

Why regulate?

For homeostasis (sustain metabolic tissue requirements-oxygen and nutrients- as per demand and waste elimination-CO2 & other products of metabolism-)

Neural

Humoral

On integration Neuro-humoral

Agents of regulation:

Purely Autonomic

-Sympathetic

-Parasympathetic

Key terms: RVLM; DVN; NTS; Carotid and Aortic sinuses

Neural

The medulla oblongata located within the brainstem, the

hypothalamus, and the cortical regions work together to regulate autonomic function.

The medulla contains the ANS centers, the hypothalamus modulates medullary activity in relation to requirements, higher cortical centers alter CVS func in relation to stress, anxiety, exercise etc

Afferent fibers from peripheral baroreceptors and

chemoreceptors, as well as respiratory stretch receptors, enter the medulla at the nucleus tractussolitarius (NTS).

The NTS relays inhibitory nerves to the

RVLM(sympathetic nervous system cell nuclei); and excitatory signals to the DVN (parasympathetic nervous system nuclei)

Therefore NTS activity = sympathetic activity and parasympathetic activity.

Cell bodies are found in collections of neurons called the

dorsal vagal nucleus (DVN) and nucleus ambiguus (NA).

activity here is associated with

reduces sinoatrial (SA) nodal firing (negative chronotropy)

slows AV nodal conduction (negative dromotropy)

NB: Increased baroreceptor firing causes excitation of these centers.

Parasympathetic innervation;

Existing parasympathetic nerves do not play a

significant role in the regulation of systemic vascular resistance and arterial blood pressure.

The sympathetic adrenergic neuron cell bodies lie

within the Rostral ventral lateral medulla (RVLM).

Increased activity of these neurons produces cardiac stimulation and systemic vasoconstriction.

Sympathetic activation increases chronotropy, dromotropy, and inotropy.

Sympathetic innervation;

Activation of one arm of the ANS is assoc with

reciprical inhibition of the other arm.

Example; Standing up causes baroreceptor reflex to reduce parasympathetic outflow and concurrent increase in sympathetic outflow. Thus sustaining normal BP despite reduced venous return.

RECIPROCAL SYMPATHETIC AND VAGAL ACTIVITY:

Input from higher centers eg sudden fear or emotion can

cause vagal stimulation and withdrawal of sympathetic tone = bradycardia and vasodilation = hypotension. Hence a vasovagal syncope.

Fear and anxiety can lead to sympathetic activation.

Chronic sympathetic activation induced by long-term emotional stress can result in sustained hypertension, cardiac hypertrophy, and arrhythmias.

Check effector receptor location & function;

Alpha and Beta receptors

Muscarine and nicotinic receptors

Arterial blood pressure is regulated through

negative feedback systems.

Arterial baroreceptors are found in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch.

Baroreceptor Feedback Regulation of Arterial Pressure:

The sinus nerve, a branch of the glossopharyngeal nerve

(cranial nerve IX), innervates the carotid sinus.

Afferent fibers from the carotid sinus synapse at the NTS. (Recall, NTS modulates the activity of sympathetic neurons within

the RVLM and medullary vagal nuclei.)

The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve prior to synapsing at NTS.

The arterial baroreceptors respond to the stretching

of the vessel walls produced by increases in arterial blood pressure which subsequently causes increeased firing.

Overall, the receptors of the carotid sinus respond to

pressures ranging from about 60 to 180 mm Hg.

If arterial blood pressure decreases from normal, it lowers the firing rate of the carotid sinus baroreceptors and vice versa.

Carotid sinus is more sensitive than aortic sinus

Scenario examples; Standing up, Carotid massage, Valsalva manouvre

The primary role of these receptors is to regulate pCO2;

pO2; pH within normal limits.

Also interact with medullary cardiovascular centers directly -hypoxic environs, poor gaseous exchange, hypotension increase

firing of nerves in RVLM- and indirectly via pulmonary stretch receptors - causes inhibition of vagal discharge from DVN-.

Central receptors also respond similarly.

Chemoreceptor Feedback Regulation of Arterial Pressure:

Pediatric bradycardia with hypoxia-

Normal response to hypoxia-

Analogy:

Some affect blood vessels and the heart directly

Others affect blood volume

Examples

circulating catecholamines

the renin-angiotensin- aldosterone system

atrial natriuretic peptide

antidiuretic hormone (vasopressin)

HUMORAL CONTROL

Circulating catecholamines originate from two

sources :

The adrenal medulla -catecholamines(80% epinephrine, 20% norepinephrine)

Sympathetic nerves innervating blood vessels (principally norepinephrine)

Circulating Catecholamines

Catecholamine activity is governed by receptor

distribution (e.g. the affinity of epinephrine for β-adrenoceptors is much greater than for α-adrenoceptors.)

Therefore, at low to moderate circulating levels of

epinephrine, heart rate, inotropy, and dromotropy are stimulated (primarily β1-adrenoceptor mediated).

At high plasma concentrations, the cardiovascular actions of epinephrine are different because epineph-rine binds to α-adrenoceptors as well as to β-adrenoceptors.

NB- Check Nor-epi receptor affinities??

Renin is primarily produced in the kidney

(Juxtaglomerular cells)

Production is dictated by;

B1 stimulation in the kidney

Renal artery hypotension

Reduced Na delivery to distal tubules

The Renin-Angiotensin-Aldosterone system

Angiotensinogen

Renin

Angiotensin I

ACE (In lung endothelium)

Angiotensin II

Constricts resistance vessels( Increasing SVR)

Enhances sympathetic adrenergic activity (Locally and centrally)

Acts upon the adrenal cortex to release aldosterone(Thus increase in blood volume)

Stimulates the release of vasopressin from the posterior pituitary

Stimulates thirst centers within the brain

Stimulates cardiac and vascular hypertrophy.

Angiotensin II actions

It is synthesized stored and released by atrial myocytes in

response to Atrial distension (think heart failure, vol, overload)

Angiotensin II

Sympathetic stimulation.

Function- Longterm regulation of Na, water ,blood vol. homeostasis.

Actions tend to be the opposite of angiotensin II action.

Atrial Natriuretic Peptide

Vassopressin(ADH)

It is released from the posterior pituitary

Action sites at kidneys and blood vessels

The most important physiologic action of AVP is that it increases water reabsorption by the kidneys.(via V2 receptors)

This hormone also constricts arterial blood vessels through V1 vascular receptors

NB: Consider all the afore mentioned as a finely tuned intergrated system working in sync not as compartments.

THE END

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