EFFECT OF INHIBITION OF CONVERTING ENZYME ON INACTIVE RENIN IN THE CIRCULATION OF SALT-REPLETE AND SALT-DEPLETE NORMAL SUBJECTS

Angiotensin II exerts an inhibitory influence on active renin release from the kidney. To assess a possible role for angiotensin II in the release of inactive renin, levels in the circulation were measured before and at regular intervals after the administration of captopril, an orally active inhibitor of angiotensin I-converting enzyme, to 12 salt-replete and six salt-deplete normal subjects. Concurrent measurements of active renin, angiotensin I and angiotensin II were also performed. Basal inactive renin in the salt-deplete group was increased compared with the salt-replete subjects, but inactive renin remained constant in both groups after treatment with captopril. There were significant increases in concentrations of both active renin and angiotensin I after treatment with captopril in all subjects and corresponding decreases in angiotensin II. These results suggested that angiotensin II does not influence the release of inactive renin, in contrast with its role in the release of active renin.

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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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-019 ◽

1984 ◽

Vol 62 (1) ◽

pp. 116-123 ◽

Cited By ~ 15

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.

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Immunoreactive angiotensin I converting enzyme in plasma from normal subjects. Comparison with enzyme activity

European Heart Journal ◽

10.1093/eurheartj/4.suppl_g.27 ◽

1983 ◽

Vol 4 (suppl G) ◽

pp. 27-29 ◽

Cited By ~ 1

Author(s):

T. Yasui ◽

F. Alhenc-Gelas ◽

S. Daufresne

Keyword(s):

Enzyme Activity ◽

Normal Subjects ◽

Converting Enzyme ◽

Angiotensin I ◽

Angiotensin I Converting Enzyme

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Angiotensin I-converting enzyme-dependent and neutral endopeptidase-dependent generation and degradation of angiotensin II contrarily modulate noradrenaline release: implications for vasopeptidase-inhibitor therapy?

Journal of Hypertension ◽

10.1097/01.hjh.0000173395.42794.cd ◽

2005 ◽

Vol 23 (8) ◽

pp. 1597-1604 ◽

Cited By ~ 2

Author(s):

Walter Raasch ◽

Peter Dominiak ◽

Andreas Dendorfer

Keyword(s):

Angiotensin Ii ◽

Noradrenaline Release ◽

Neutral Endopeptidase ◽

Inhibitor Therapy ◽

Converting Enzyme ◽

Angiotensin I ◽

Angiotensin I Converting Enzyme ◽

Vasopeptidase Inhibitor

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Thirst and brain angiotensin in cattle

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.2.r204 ◽

1992 ◽

Vol 262 (2) ◽

pp. R204-R210

Author(s):

J. R. Blair-West ◽

D. A. Denton ◽

M. J. McKinley ◽

R. S. Weisinger

Keyword(s):

Angiotensin Ii ◽

Water Intake ◽

Enzyme Inhibitors ◽

Converting Enzyme ◽

Preoptic Nucleus ◽

Angiotensin I ◽

Converting Enzyme Inhibitors ◽

Median Preoptic Nucleus ◽

Angiotensin I Converting Enzyme ◽

Reduced Water

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.

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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

Clinical Science ◽

10.1042/cs0580445 ◽

1980 ◽

Vol 58 (6) ◽

pp. 445-450 ◽

Cited By ~ 26

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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