scholarly journals Effects of angiotensin I converting enzyme inhibitor (SQ 14,225) on the responses of blood pressure and steroid hormone to angiotensin II and ACTH infusion in hypertensive subjects.

1982 ◽  
Vol 46 (3) ◽  
pp. 267-273 ◽  
Author(s):  
YASUHISA UEDA ◽  
MASANOBU HONDA ◽  
MICHlNOBU HATANO
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Steroid Hormone ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Converting Enzyme Inhibitor ◽  
Angiotensin I Converting Enzyme

Effects of angiotensin I converting enzyme inhibitor (SQ 14225) on control of aldosterone

1980 ◽  
Vol 94 (2) ◽  
pp. 213-220 ◽  
Author(s):  
Toyohisa Eguchi ◽  
Ikuo Saito ◽  
Ryuichi Nakamura ◽  
Toshiyuki Yasui ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Inhibitory Effect ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Converting Enzyme Inhibitor ◽  
Angiotensin I Converting Enzyme ◽  
Pre Treatment ◽  
Remarkable Reduction

Abstract. To study effects of angiotensin I converting enzyme inhibitor (CEI), SQ 14225, on plasma aldosterone (PA), angiotensin I (AI), angiotensin II (AII), potassium and ACTH were administered with or without the simultaneous injection of SQ 14225 in rabbits. The direct effect of bradykinin on PA was also examined, since it is suspected to augment the action of kinin under the administration of CEI. In rabbits the dose of 1 mg/kg of SQ 14225 by a bolus injection resulted in a marked elevation of plasma renin activity (PRA) and moderate but significant decreases in circulating AII and PA with only a little change of blood pressure. Decrements in circulating AII and those in PA observed after the injection of SQ 14225 were well correlated (r = 0.585, P < 0.05). Stimulatory effects of AII, potassium and ACTH on PA were not affected by SQ 14225, however, those of AI on PA and blood pressure were completely inhibited by pre-treatment of SQ 14225. The infusion of bradykinin showed a remarkable reduction in blood pressure and a small increment in PRA, circulating AII and PA. These results may suggest that the inhibitory effect of acutely administered SQ 14225 on PA is mainly due to the inhibition of conversion from AI to AII, but not direct effects on adrenal glands. Furthermore, it was suggested that the augmented kinin is not related to the inhibitory effect of SQ 14225 on PA. In addition, the administration of SQ 14225 does not change the effects of potassium and ACTH on PA.

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.

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