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DRUG USED TO TREAT HIGH BLOOD PRESSURE

Depending on their mechanism of action, the different drugs used to treat hypertension belong

to several classes. These classes are:

Preferred Agents

 Diuretics

 Beta-adrenergic blocking agents

Alternative Agents

 Angiotensin-converting enzyme inhibitors

 Angiotensin II receptor antagonists

 Calcium ion antagonists

 Alpha-I adrenergic

Adjunctive Agents

 Central acting-2 agonists

 Peripheral-acting adrenergic antagoninsts

 Direct vasodilators

Drug Class: Diuretics

Action:

Diuretics acts by causing volume reduction, sodium excretion, and vasodilation of peripheral

arterioles. The mechanisms for peripheral arteriolar vasodilation is unknown.

Uses:

There are four class of diuretics


 Carbonic anhydrase inhibitors ( have weak antihypertensive effects, so they are not

used for this purpose)

 Thiazide and thiazide-like agents

 Loop diuretics

 Potassium-sparing diuretics ( rarely used alone, these are usually combined with

thiazides and loop diuretics for added antihypertensive effects and to counteract the

potassium excreting effects of more potent diuretic-antihypertensive)

Diuretics are the most commonly used prescribed antihypertensive agents because they

reduce morbidity and mortality associated with hypertension. The thiazides are the most

effective if the renal creatinine clearance is greater than 30 mL per minute. As renal function

deteriorates, the more potent loop diuretics are used to continue excretion of sodium and water.

Diuretics are also commonly prescribed in combination with other drugs. They potentiate

the hypotensive activity of the non-diuretic antihypertensive drugs, have a low incidence of

adverse effects, and are often the last expensive of the hypertensive drugs. A more complete

discussion of diuretics is given in chapter 30.

Drug Class: Beta-Adrenergic Blocking Agents

Action

The beta-blockers (refer to table 14-3) inhibit cardiac response to sympathetic nerve

stimulation by blocking the beta-receptors. This produces a reduction in heart rate. Cardiac

output, and blood pressure.

Uses

The ACE inhibitors reduce blood pressure, preserve cardiac output, and increase renal

blood flow. They are effective as single therapy for Stages 1 or 2 hypertension, severe

accelerated hypertension, and renal hypertension. The JNC-6 considers them as an alternative
to diuretics and beta-blockers. Although, they may be used alone, they are more effective when

combined with diuretic therapy. They are not as effective in lowering blood pressure in

African-Americans unless used with a diuretic. The ACE inhibitors are also effective in the

treatment of heart failure and may be useful in slowing the progression of diabetic neuropathy.

The advantages of ACE inhibitors are the infrequency of orthostatic hypotension; lack

of CNS depression and sexual dysfunction side effects; lack of aggravation of asthma,

obstructive pulmonary disease, gout, high cholesterol levels, or diabetes; and, an additive effect

with diuretics.

Side Effects to Expect and Report

Side effects include mild nausea, and fatigue, orthostatic hypotension with mild

dizziness, weakness, and faintness.

Report swelling of the face, eyes, lips, tongue, difficulty in breathing, and angioedema;

neutropenia (300 neutrophils/mmᶟ) and agranulocytosis (drug induced bone marrow

suppression)

Patients at risk are those receiving captopril and who have impaired renal function or

serious autoimmune diseases such as lupus erythematosus, or those who are exposed to drugs

known to affect the white cells or immune response, such as corticosteroids. A number of

patients, especially those with pre-existing renal impairment, may develop increase in BUN

and serum creatinine, indicating the possibility of neurotoxicity. Because ACE inhibitors

inhibit aldosterone, patients may develop slight increases in serum potassium (hyperkalemia).

Many patients receiving ACE inhibitors develop a chronic dry, non-productive cough believed

to be caused by accumulation of bradykinin.

Medicines that act directly on the renin angiotensin system can cause fetal and neonatal

harm because of increased risk of birth defects.

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