Hormonal Changes with Long-Term Converting-Enzyme Inhibition by Captopril in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 135s-138s ◽  
Author(s):  
P. G. Matthews ◽  
B. P. McGrath ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Diuretic Therapy ◽  
Plasma Renin ◽  
Hormonal Changes ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Plasma Angiotensin ◽  
Converting Enzyme Inhibition

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.

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
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibition ◽  
Plasma Renin ◽  
Converting Enzyme ◽  
Blood Pressure Elevation ◽  
Antihypertensive Action ◽  
Plasma Angiotensin ◽  
Converting Enzyme Inhibition ◽  
Sodium And Potassium

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.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

The Effect of Captopril on Blood Pressure and Angiotensins I, II and III in Sodium-Depleted Dogs: Problems Associated with the Measurement of Angiotensin II after Inhibition of Converting Enzyme

1980 ◽  
Vol 58 (6) ◽  
pp. 445-450 ◽  
Author(s):  
J. J. Morton ◽  
M. Tree ◽  
J. Casals-Stenzel
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Fold Increase ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Active Inhibitor ◽  
Arterial Blood ◽  
Rapid Fall ◽  
Angiotensin Iii ◽  
Plasma Angiotensin

1. Changes in arterial blood pressure, blood angiotensin I, plasma angiotensin II and plasma angiotensin III were measured in conscious sodium—depleted dogs after infusion of captopril, an orally active inhibitor of converting enzyme. 2. Angiotensins II and III were measured after chromatography to remove angiotensin I, which increased in concentration after inhibition of converting enzyme and which interfered in the direct assay for angiotensin II. 3. Infusion of captopril at 20, 200, 2000 and 6000 μg h−1 kg−1, each for 3 h, produced a rapid fall in blood pressure and in concentration of angiotensin II. Angiotensin II was undetectable at 6000 μg h−1 kg−1 (mean pre-infusion value for all samples was 39 ± sd 15 pmol/I, n = 14) 4. The percentage fall in blood pressure correlated with the percentage fall in plasma angiotensin II (r = 0.65, P<0.001) 5. These results suggest that the initial fall in blood pressure may be mediated in part by the suppression of angiotensin II. 6. Blood angiotensin I concentration rose with each rate of infusion of drug to a maximum 16-fold increase at 6000 μg h−1 kg−1 (26−416 pmol/l). The rise in angiotensin I was inversely related to the fall in angiotensin II (r = −0.68, P<0.001)

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