By : Abeer ahmed

Hypertension medications

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hypertension pathology :• The force of the blood is constantly putting pressure on the

walls of blood vessels this is known as “blood pressure”.• Blood pressure is regulated by chemicals in the body that

change the diameter of the blood vessel depending on the needs of the body through vasoconstriction or vasodilata-tion .

Untreated hypertension may cause :

Ace inhibitors :• A chemical that is present on the wall of blood vessels called angiotensin 1 binds to an enz called angiotensin converting enz

(ACE).• Angiotensin I in the blood is itself formed from angiotensinogen,

a protein produced by the liver and released into the blood

• once bound a new chemical called angiotensin 2 is created .• Angiotensin 2 binds to receptors on the smooth muscles of the blood vesseles leading them to narrow (vasoconstriction) .

Figure showing ace inhibitors “the pink one “ blocking the active site of angiotensin converting enzyme .This prevents the chemical converion of angiotensin 1 to an-giotensin2 .

The following is a list of the ACE inhibitors :• benazepril (Lotensin)• captopril (Capoten)• enalapril (Vasotec, Epaned)• fosinopril (Monopril)• lisinopril (Prinivil, Zestril) • moexipril (Univasc)• perindopril (Aceon) • quinapril (Accupril) • ramipril (Altace)• trandolapril (Mavik)

What are the side effects of ACE inhibitors?

• ACE inhibitors usually are not prescribed for pregnant women because they may cause birth defects.

• Individuals with bilateral renal artery stenosis (narrowing of the

arteries that supply the kidneys) may experience worsening of

kidney function.• It may take up to a month for coughing to subside, and if

one ACE inhibitor causes cough it is likely that the others will too.

• ACE inhibitors may increase blood levels of potassium and cause

hyperkalemia.• ACE inhibitors also may increase the blood concentration of

lithium .• There have been reports that nonsteroidal anti-inflammatory

drugs (NSAIDS) may reduce the blood pressure lowering effects of ACE inhibitors.

• Patients receiving diuretics may experience excessive reduction in

blood pressure when ACE inhibitors are started. Stopping the di-uretic or increasing salt intake prior to taking the ACE inhibitor may prevent

excessive blood pressure reduction.

• ACE inhibitors should not be combined with ARBs because such

combinations increase the risk of hypotension, hyperkalemia, and

renal impairment.

Mechanism of interaction between diuretics and ACEI• Diuretics can reduce plasma volume leading to re-

duced renal blood flow. This may lead to increased serum crea-

tinine concentrations.• The kidney can compensate via the renin-angiotensin system by constricting the efferent renal arteriole to in-

crease glomerular filtration pressure and favor water and

sodium retention

Mechanism of NSAIDs interaction with ACEI• NSAIDs, by inhibition of prostaglandins and bradykinin,

produce vasoconstriction of the afferent renal arteriole.

For what conditions are ACE inhibitors used?

• controlling acute and chronic high blood pressure

• treating left ventricular dysfunction and heart failure.• preventing strokes.• preventing and treating kidney disease (nephropathy) in people with hypertension or diabetes.

ARBs mechanism of action

• angiotensin II receptor antagonists work By at-taching

to AT1 receptors on smooth muscle cells lining the blood vessels, this drug blocks angiotensin II from binding.

The following is a list of currently available ARBs:

• azilsartan (Edarbi)• candesartan (Atacand),• eprosartan (Teveten),• irbesartan (Avapro),• telmisartan (Micardis),• valsartan (Diovan),• losartan (Cozaar), and • olmesartan (Benicar).

Adrenergic receptors :

Alpha-Adrenergic Blockers:

• Norepinephrine is released from the adrenal gland where it circulates in the bloodstream and binds to proteins,

called alpha-adrenergic receptors, on the surface of smooth muscles within the blood vessels.

• Once bound, the smooth muscle cells tighten, de-creasing the width of the blood vessel.

Alpha adrenergic blockers MOA :• alpha-adrenergic blockers act By selectively attach-

ing to alpha-adrenergic receptors on smooth muscle cells lining the blood vessels, this drug blocks norep-inephrine from binding.

Examples of non-selective α-adrenergic re-ceptor antagonists include:• Phenoxybenzamine• Phentolamine• Tolazoline• Trazodone• Typical and atypical antipsychotics

Selective α1-adrenergic receptor antagonists include

• Alfuzosin• Doxazosin• Prazosin (inverse agonist)• Tamsulosin• Terazosin• Silodosin[

Selective α2-adrenergic receptor antagonists include :• Atipamezole• Idazoxan• Mirtazapine• Yohimbine• carvedilol and labetalol are both α- and β-blockers.