Captopril in Hypertension with Renal Artery Stenosis and in Intractable Hypertension; Acute and Chronic Changes in Circulating Concentrations of Renin, Angiotensins I and II and Aldosterone, and in Body Composition

Abstract

1. The converting-enzyme inhibitor captopril has been given in doses up to 450 mg daily to hypertensive patients with renal artery stenosis and to patients resistant to other therapy. 2. Captopril alone was effective in controlling hypertension in renal artery stenosis, irrespective of whether pretreatment plasma angiotensin II was raised or normal, except in one man with overall renal impairment. 3. In one woman with the hyponatraemic hypertensive syndrome secondary to renal artery thrombosis, captopril restored depleted exchangeable sodium and potassium to normal. In the other cases of renal artery stenosis with normal renal function, exchangeable sodium and total body potassium were not significantly altered, and there were no marked changes in plasma sodium and potassium. 4. The combination of captopril with a diuretic controlled blood pressure long-term in every case of previously resistant hypertension. 5. Within 2 h, captopril induced highly significant falls in arterial pressure, in plasma angiotensin II and aldosterone, with converse increases in plasma active and total renin and blood angiotensin I. 6. The initial fall in plasma angiotensin II was closely related to the concomitant fall in diastolic pressure. 7. The pattern of change in circulating renin, angiotensins I and II and aldosterone was maintained during long-term therapy, whether or not a diuretic was added. There was no tendency for plasma angiotensin II to increase despite sustained elevation of active renin and angiotensin I.

Time Course of Changes in Blood Pressure, Aldosterone and Body Fluids During Enalapril Treatment: A Double‐blind Randomized Study vs Hydrochlorothiazide Plus Propranolol in Essential Hypertension

“…In agreement with previous reports (Atkinson et al 1979;Tarazi el al. 1980;de Leeuw et al 1983;Omvik & Lund-Johansen 1984), after 6 weeks of treatment extracellular fluid volumes were similar to those before drug administration.…”

“…Various mechanisms have been postulated to be involved in the blood pressure lowering effect of angiotensin converting enzyme inhibition, namely a reduction in circulating angiotensin I1 (Atkinson et al 1979;, increased levels of vasodilatory prostaglandins (Swartz et al 1979(Swartz et al , 1980Abe et al 1980;Witzgall et al 1982;Rossi et al 1984) and renal kinins (Anderson et al 1980;Clappison et al 1981), a reduction in angiotensin I1 within the central nervous system (Mann et al 1979) and a reduction in aldosterone production with ensuing natriuresis (Atlas et al 1979;Maitra et al 1981). This latter action is said to operate mainly in the long-term, but measurement of body fluids and sodium balance in hypertensive patients chronically treated with converting enzyme inhibitors have given conflicting results.…”

Sustained Antihypertensive Effect of Captopril Combined with Diuretics and Beta‐adrenergic Blocking Drugs in Patients with Resistant Hypertension

“…Relatively few reports have been published on longterm antihypertensive effect of captopril in the treatment of resistant hypertension (5)(6)(7)(8)(9). This report is mainly codirmative and includes patients treated with captopril in addition to /3-adrenergic blocking drugs and diuretics during a one-year follow-up period.…”

Inhibitors of angiotensin I converting enzyme for treating hypertension.

“…'517 While the immediate drop in pressure is closely related to the extent of the fall in plasma angiotensin II this does not necessarily confirm a simple cause-effect mechanism. 8 If exogenous angiotensin II is infused after administration of teprotide or captopril a higher plasma concentration of angiotensin II has to be attained than before treatment in order to restore the blood pressure to control values.6 18 Hence there are components ofthe antihypertensive action in addition to the effect on angiotensin II. Further evidence is provided by the lowering of blood pressure by captopril in sodium-depleted anephric patients,'9 though the significance of this finding has been disputed.20 Converting enzyme is one of the enzymes which metabolise the vasodilator peptide bradykinin,21 and hence inhibitors of converting enzyme might in part lower blood pressure by prolonging the survival of bradykinin.…”