Converting Enzyme Inhibition during Chronic Angiotensin II Infusion in Rats: Evidence against a Non-Angiotensin Mechanism

1980 ◽  
Vol 59 (s6) ◽  
pp. 71s-74s ◽  
Author(s):  
S. C. Textor ◽  
H. R. Brunner ◽  
H. Gavras

1. To investigate the non-angiotensin effects of converting enzyme inhibition, angiotensin II was infused intravenously at 30 ng/min for 9 days in conscious rats to produce moderate blood pressure elevation. One group was given captopril (SQ 14 225) by gavage (100 mg/kg twice daily) and the other glucose. 2. After 7 days of captopril administration, enzyme blockade was confirmed by a tenfold greater depressor sensitivity to exogenous bradykinin and a markedly decreased plasma angiotensin converting enzyme activity. 3. Mean arterial pressure, heart rate and plasma renin activity were not different between captopril and glucose-treated groups in the presence of angiotensin II. Metabolic studies also revealed no long-term differences in water and food intake, weight change or sodium and potassium metabolism. 4. These findings suggest that, in the presence of angiotensin II, there is no detectable haemodynamic or metabolic effect of converting enzyme inhibition in rats and, therefore, that bradykinin plays little or no role in its long-term antihypertensive action.

1979 ◽  
Vol 57 (s5) ◽  
pp. 135s-138s ◽  
Author(s):  
P. G. Matthews ◽  
B. P. McGrath ◽  
C. I. Johnston

1. Captopril was shown to be as effective as hydrochlorothiazide in lowering the blood pressure in patients with moderately severe essential hypertension. 2. With the combination of captopril and hydrochlorothiazide satisfactory control of blood pressure was maintained over 8 months. 3. Inhibition of angiotensin converting enzyme by captopril in man was associated with falls in plasma angiotensin II and urinary aldosterone and rises in angiotensin I and plasma renin. 4. No change in venous concentrations of bradykinin could be demonstrated during therapy. 5. Captopril attenuated the hyperaldosteronism and hypokalaemia associated with diuretic therapy.


1987 ◽  
Vol 72 (3) ◽  
pp. 387-389 ◽  
Author(s):  
J. Nussberger ◽  
D. B. Brunner ◽  
B. Waeber ◽  
J. Biollaz ◽  
Hans R. Brunner

1. In nine normal volunteers, a series of five venous blood samples was obtained before and up to 24 h after converting enzyme inhibition by a single oral dose of enalapril or lisinopril. Plasma renin activity and blood angiotensin I were measured. 2. A close linear relationship was found between the increase in plasma renin activity and the increase in blood angiotensin I. 3. The linear correlation between plasma renin activity and blood angiotensin I remained after converting enzyme inhibition. 4. Thus, the rise in angiotensin I after inhibition of the conversion of angiotensin I to angiotensin II is due to an enhanced release of renin rather than to accumulation of angiotensin I.


Hypertension ◽  
2002 ◽  
Vol 40 (6) ◽  
pp. 840-846 ◽  
Author(s):  
Dominik N. Muller ◽  
Alexander Mullally ◽  
Ralf Dechend ◽  
Joon-Keun Park ◽  
Anette Fiebeler ◽  
...  

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