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帕吉林对自发性高血压大鼠降压作用的中枢介导

Central mediation of the antihypertensive effect of pargyline in spontaneously hypertensive rats.

作者信息

Fuentes J A, Ordaz A, Neff N H

出版信息

Eur J Pharmacol. 1979 Jul 15;57(1):21-7. doi: 10.1016/0014-2999(79)90099-2.

DOI:10.1016/0014-2999(79)90099-2
PMID:477738
Abstract

The monoamine oxidase (MAO) inhibitor pargyline induced a moderate (about 20 mm Hg) but persistent (48 h) decrease of systolic blood pressure in unanesthetized adult spontaneously hypertensive rats (SHR) but not in normotensive rats. The fall of blood pressure correlated with the blockade of norepinephrine (NE) deamination by brain homogenates. After an intracerebroventricular (icv) injection of 6-hydroxydopamine, which lowered brain NE content by about 70%, pargyline was unable to diminish arterial pressure. Blockade of central alpha-adrenoceptors by treatment with phentolamine (100 microgram icv) could either prevent or reverse the fall of blood pressure in SHR induced by pargylline. Moreover, a low dose of pargyline injected directly into the brain lowered arterial pressure. We conclude that the hypotensive action of pargylline in SHR appears to be the consequence of NE accumulating at an inhibitory alpha-adrenoceptor in brain.

摘要

单胺氧化酶(MAO)抑制剂帕吉林可使未麻醉的成年自发性高血压大鼠(SHR)的收缩压适度(约20 mmHg)但持续(48小时)下降,而对正常血压大鼠则无此作用。血压下降与脑匀浆对去甲肾上腺素(NE)脱氨基作用的阻断相关。脑室内(icv)注射6-羟基多巴胺使脑NE含量降低约70%后,帕吉林无法降低动脉血压。用酚妥拉明(100微克icv)治疗阻断中枢α-肾上腺素能受体,可预防或逆转帕吉林所致SHR的血压下降。此外,直接注入脑内的低剂量帕吉林可降低动脉血压。我们得出结论,帕吉林在SHR中的降压作用似乎是NE在脑内抑制性α-肾上腺素能受体处蓄积的结果。

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Central mediation of the antihypertensive effect of pargyline in spontaneously hypertensive rats.帕吉林对自发性高血压大鼠降压作用的中枢介导
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Treatment with clorgyline and pargyline differentially decreases clonidine-induced hypotension and bradycardia.用氯吉兰和帕吉林治疗分别降低可乐定引起的低血压和心动过缓。
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