Effects of the Oral Angiotensin-Converting Enzyme Inhibitor MK-421 in Human Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 281s-283s ◽  
Author(s):  
H. Gavras ◽  
J. Biollaz ◽  
B. Waeber ◽  
H. R. Brunner ◽  
Gavras Irene ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Pressure Control ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Blood Pressure Fall ◽  
Plasma Angiotensin

1. The effects of the new oral angiotensin-converting enzyme (ACE) inhibitor MK-421 on blood pressure, plasma renin activity, angiotensin II, aldosterone and converting enzyme activity were assessed in 16 hypertensive patients followed for 6–18 weeks. 2. After an initial titration period, maintenance doses of 2.5–40 mg once daily produced satisfactory blood pressure control in 11 and a partial but significant decrease in the remainder. 3. Treatment was associated with no change in heart rate and no orthostatic hypotension. At 24 h after the first effective dose, blood pressure was still decreased, plasma ACE was suppressed to 16% of the baseline, plasma angiotensin to 58%, aldosterone to 42%, and plasma renin activity was elevated to 228% of the baseline. 4. Magnitude of blood pressure fall was significantly correlated with the height of pretreatment blood pressure but not with baseline levels of plasma renin activity.

Effect of Angiotensin II and Converting Enzyme Inhibitor (Captopril) on Blood Pressure, Plasma Renin Activity and Aldosterone in Primary Aldosteronism

1981 ◽  
Vol 61 (s7) ◽  
pp. 289s-293s ◽  
Author(s):  
F. Mantero ◽  
F. Fallo ◽  
G. Opocher ◽  
D. Armanini ◽  
M. Boscaro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Idiopathic Hyperaldosteronism

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma and urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Effect of the Converting-Enzyme Inhibitor SQ 14 225 (captopril) in Early One-Kidney, One-Clip Hypertension in the Rat

1981 ◽  
Vol 60 (4) ◽  
pp. 387-392 ◽  
Author(s):  
R. Vandongen ◽  
Anne Tunney ◽  
Patricia Martinez
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Hypotensive Action ◽  
Converting Enzyme Inhibitor ◽  
Restore Blood Pressure ◽  
Arterial Plasma

1. Arterial plasma renin activity was significantly elevated in rats with one-kidney, one-clip hypertension of less than 3 weeks duration. 2. Intraperitoneal injection of the angiotensin-converting enzyme inhibitor SQ 14 225 (captopril) caused a dose-related decrease in systolic blood pressure in hypertensive rats. The lowest dose of captopril used (3.5 mg/kg) inhibited conversion of exogenous angiotensin I and maximally potentiated the depressor response to bradykinin, but failed to restore blood pressure to that of the normotensive controls. 3. Removal of the solitary clipped kidney also did not restore blood pressure to normal. Injection of captopril (3.5 mg/kg) 24 h after nephrectomy, when no circulating renin activity was detectable, lowered blood pressure further in hypertensive but not in similarly nephrectomized controls. 4. These results indicate that raised blood pressure in early one-kidney, one-clip hypertension in the rat cannot be entirely attributed to the renin-angioterisin system, even when plasma renin activity is significantly increased. 5. This study has also confirmed a hypotensive action of captopril in anephric rats when plasma renin activity is undetectable.

Blood Pressure Response of Nephrectomized Hypertensive Rats to Converting Enzyme Inhibition: Evidence for Persistent Vascular Renin Activity

1977 ◽  
Vol 52 (3) ◽  
pp. 299-304 ◽  
Author(s):  
H. Thurston ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Bilateral Nephrectomy ◽  
Hypertensive Rats ◽  
Angiotensin System

1. Blood pressure and plasma renin activity were studied after bilateral nephrectomy in groups of rats with hypertension caused by unilateral renal ischaemia with the opposite kidney left intact. 2. Although blood pressure showed only a small fall in the first hour after bilateral nephrectomy, plasma renin activity fell rapidly with a half-life of 10 min. 3. Infusion of converting enzyme inhibitor (SQ20881) produced a 26·1% fall in blood pressure 1 h after nephrectomy, 24·0% at 2 h and 4·6% at 6 h. 4. An angiotensin antagonist (Sar1-Ala8-angiotensin II) was infused into hypertensive rats 1 h after nephrectomy; this blocked the vasodepressor action of the converting enzyme inhibitor, indicating that the fall in blood pressure produced by the inhibitor was due to its action upon the renin-angiotensin system. 5. The renin—angiotensin system maintains blood pressure in this model even after plasma renin has fallen to insignificant levels. This supports the view that vascular renin activity has a longer half-life than circulating renin and is important in the control of blood pressure.

Sign in / Sign up

Export Citation Format

Share Document