Effect of captopril on converting enzyme activity in chemically sympathectomized, spontaneously hypertensive rats.
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概要
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Effect of subacute angiotensin converting enzyme (ACE) blockade on the converting enzyme activity (ACE activity) in plasma, aorta, lung, kidney and whole brain was evaluated in chemically-sympathectomized (with 6-hydroxydopamine) normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) using captopril given peripherally via the intraperitoneal (i.p) route and centrally through intracerebroventricular (l.c.v.) administration. Daily i.p. injection of 25 mg/kg for 8 days reduced the blood pressure of both WKY rats and SHR, and the ACE activity in the aorta, lung and plasma of both WKY rats and SHR were correspondingly depressed. The brain ACE activity remained unaltered in both strain of rats. The ACE activity in the kidney of WKY was depressed, while that of SHR remained unchanged. These observations are independent of peripheral sympathectomy with 6-hydroxydopamine (6-OHDA). Daily central captopril administration at a dose of 2 mg/kg, i.c.v., for 8 days significantly reduced the blood pressure of SHR but not WKY rats, whereas the ACE activity of the whole brain of both WKY and SHR were depressed. Central sympathectomy with 6-OHDA did not alter these responses. It is concluded that captopril exerts its antihypertensive effect not only via reduction of the ACE activity in the plasma and lungs as reported earlier, but also that of other organs, principally the aorta, and that these effects are independent of the sympathetic nervous system.
- 公益社団法人 日本薬理学会の論文
著者
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SATTAR Munavvar
School of Pharmaceutical Sciences, Universiti Sains Malaysia
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LATIFF Aishah
School of Pharmaceutical Sciences, Universiti Sains Malaysia
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GAN Ee-Kiang
School of Pharmaceutical Sciences, Universiti Sains Malaysia
関連論文
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- Effect of captopril on converting enzyme activity in chemically sympathectomized, spontaneously hypertensive rats.
- Effect of chronic angiotensin-converting enzyme blockade on pressor responses to exogenous angiotensin II, noradrenaline and vasopressin in deoxycorticosterone acetate salt (DOCA)-induced hypertensive rats.