Enalapril in the treatment of hypertension with renal artery stenosis.

Abstract

The converting enzyme inhibitor enalapril, in single daily doses of 10-40 mg, was given to 20 hypertensive patients with renal artery stenosis. The blood pressure fall six hours after the first dose of enalapril was significantly related to the pretreatment plasma concentrations of active renin and angiotensin II and to the concurrent fall in angiotensin II. Blood pressure fell further with continued treatment; the long term fall was not significantly related to pretreatment plasma renin or angiotensin II concentrations. At three months, 24 hours after the last dose of enalapril, blood pressure, plasma angiotensin II, and converting enzyme activity remained low and active renin and angiotensin I high; six hours after dosing, angiotensin II had, however, fallen further. The rise in active renin during long term treatment was proportionally greater than the rise in

An overview of the clinical pharmacology of enalapril.

“…Because of the high levels of plasma angiotensin I measured during long-term ACE inhibition , concern has been expressed about crossreactivity of angiotensin I and angiotensin II in the laboratory assay as a possible explanation for higher than expected plasma angiotensin II values. This has been excluded by both Brunner et al (1983) andHodsman et al (1983b).…”

“…However, angiotensin I did not increase in proportion, which probably reflected a fall in renin substrate with prolonged converting enzyme inhibition (Hodsman et al, 1984). Hodsman et al (1983a, b) measured the effects of enalapril in patients with renovascular hypertension and related the effects of converting enzyme inhibition, reduction of angiotensin II and aldosterone, and increases in angiotensin I levels and active renin to the reductions in blood pressure ( Figure 6). Six hours after the initial dose, blood pressure was reduced, converting enzyme was inhibited, and plasma angiotensin II levels were reduced.…”

A dose‐response study of HOE 498, a new non‐sulphydryl converting enzyme inhibitor, on blood pressure, pulse rate and the renin‐ angiotensin‐aldosterone system in normal man.

“…Angiotensin converting enzyme (ACE) inhibi-introduction of longer acting non-sulphydryl tors have proved effective therapy for hyperten-containing ACE-inhibitors, with potentially less sion (Atkinson & Robertson, 1979;Brunner et toxicity (Dollery, 1983), seems likely to widen Hodsman et al, 1983a) and heart the indications for ACE-inhibitors (Ball & failure (Atkinson & Robertson, 1979;Dargie et Robertson 1985Robertson ). al, 1983Wenting et al, 1983).…”

Use of the converting enzyme inhibitor enalapril in renovascular hypertension. Effect on blood pressure, renal function, and the renin-angiotensin-aldosterone system.

“…'• 7 Since the renin-angiotensin system plays a crucial part in the regulation of glomerular filtration rate when renal perfusion pressure is low, and short-term administration of a converting enzyme inhibitor destroys the integrity of this system, administration of a converting enzyme inhibitor to a patient with renovascular hypertension carries the risk of precipitating serious renal dysfunction. Indeed, " 23 and enalapril 8 -'• 24 have been reported to precipitate serious deterioration in glomerular filtration rate, renal plasma flow, and renal blood flow in patients with critical bilateral renal artery stenosis, renal artery stenosis in the solitary kidney, and renal artery stenosis in the transplanted kidney. Furthermore, it has been suggested that converting enzyme inhibitors invariably worsen the already impaired function of the affected kidney, 9 which raises questions concerning the potential safety of these two drugs in patients with renovascular hypertension.…”