Captopril aldosterone

More specific laboratory tests are used to diagnose secondary hypertension. These include plasma norepinephrine and urinary metanephrine levels for pheochromocytoma, plasma and urinary aldosterone levels for primary aldosteronism, and plasma renin activity, captopril stimulation test, renal vein renins, and renal artery angiography for renovascular disease. 

Like captopril, enalapril selectively suppresses the rennin-angiotensin-aldosterone system, inhibits angiotensin-converting enzyme, and prevents conversion of angiotensin I into angiotensin 11. 

The hypotensive response to captopril is accompanied by a fall in plasma aldosterone and angiotensin II levels and an increase in plasma renin activity. Serum potassium levels are not affected unless potassium supplements or potassium-sparing diuretics are used concomitantly this can result in severe hyperkalemia. 

Captopril, as well as other ACE inhibitors, is indicated in the treatment of hypertension, congestive heart failure, left ventricular dysfunction after a myocardial infarction, and diabetic nephropathy. In the treatment of essential hypertension, captopril is considered first-choice therapy, either alone or in combination with a thiazide diuretic. Decreases in blood pressure are primarily attributed to decreased total peripheral resistance or afterload. An advantage of combining captopril therapy with a conventional thiazide diuretic is that the thiazide-induced hypokalemia is minimized in the presence of ACE inhibition, since there is a marked decrease in angiotensin Il-induced aldosterone release. 

Aldosterone antagonists Captopril, potassium supplements. Hyperkalaemia. 

Captopril, many others Inhibit angiotensin converting enzyme Reduce angiotensin II levels reduce vasoconstriction and aldosterone secretion increase bradykinin Hypertension heart failure, diabetes Oral Toxicity Cough, angioedema teratogenic... 

Captopril is designated chemically as l-[(2S)-3-mercapto-2-methylpropionyl]-L-proline (14) (Fig. 8). It is used as an antihypertensive agent through suppression of the renin-angiotensin-aldosterone system [36,37], Captopril and other compounds such as enalapril and lisinopril prevent the conversion of angiotensin I to angiotensin II by inhibition of ACE. 

A test dose should be given to patients who are in cardiac failure (or who are already taking a diuretic for another reason, e.g. hypertension). Maintenance of blood pressure in such individuals may depend greatly on an activated renin-angiotensin-aldosterone system and a standard dose of an ACE inhibitor can cause a catastrophic fall in blood pressure. Except for captopril, most ACE inhibitors (including enalapril) are prodrugs, which are inactive for several hours after dosing. This has favoured the use of captopril... 

The determination of plasma renin responsiveness, however, is not sufficient to diagnose primary aldosteronism because suppressed PRA also occurs in about 25% of patients with essential hypertension. Primary aldosteronism can be differentiated from other hypermineralocorticoid states on the basis of inappropriate secretion of aldosterone. The demonstration of an elevated concentration of aldosterone in blood or urine in a patient with an unequivocally suppressed PRA concentration (a plasma aldosterone/ plasma PRA ratio >50) is presumptive evidence of primary aldosteronism. Because hypokalemia has a suppressive effect on aldosterone secretion, the potassium deficit should be replaced before aldosterone measurements are done. To establish aldosterone autonomy, the clinician may attempt to suppress aldosterone production with rapid volume expansion (see Box 51-10), with a potent mineralocorticoid (see Box 51-11), or as mentioned with captopril. Failure... 

Case, D. B., Atlas, S. A., Laragh, J. H., Sealey, J. E., Sullivan, P. A., McKinstry, D. N. Clinical experience with blockade of the renin-angi-otensin-aldosterone system by an oral converting-enzyme inhibitor (SQ 14,225, captopril) in hypertensive patients. Prog. Cardiovasc. Dis. 1978,21,195-206. 

ACE inhibitors (ACEIs) (e.g., captopril) inhibit kininase II (angiotensin-converting enzyme), blocking the formation of angiotensin II and preventing its activation of AT-1 receptors in the adrenal cortex —> 4, aldosterone and its effect on vasculature, thereby i vasoconstriction. ACEIs also inhibit the metabolism of bradykinin (BK), which causes NO/EDRF-mediated vasodilation - l TPR. 

Captopril competitively inhibits angiotensin I-converting enzyme, resulting in the prevention of angiotensin I conversion to angiotensin II, a potent vasoconstrictor that also stimulates aldosterone secretion. This action results in a decrease in sodium and fluid retention, increase in diuresis, and a decrease in BP. 

ACE inhibitors (e.g., captopril, enalapril, lisinopril, etc.) compete with angiotensin I for binding of ACE, thus reducing the formation of angiotensin II. This results in decreased vasoconstriction. Secretion of aldosterone is also reduced, resulting in decreased fluid volume, and vasodilatation is promoted through an inhibition of the metabolism of bradykinin, a potent vasodilator. This produces a net vasodilatation, accompanied by a decrease in plasma volume, resulting in a fall in blood pressure. 

Captopril, l-[(2S)-3-mercapto-2-methyl-propionyl]-L-proline, the first orally active inhibitor of the angiotensin-converting enzyme (ACE) on the market. The positive effects of captopril and other ACE inhibitors like enalapril in hypertension and heart failure result primarily from suppression of the renin-angiotensin-aldosterone system. Captopril causes a fall in blood pressure in hypertensive patients [M. A. Ondetti et al.. Science 1977,196,441 ... 

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