激肽释放酶-激肽系统未参与α-甲基多巴对正常血压大鼠的降压作用。

Lack of involvement of the kallikrein-kinin system in the depressor effect of alpha-methyldopa in normotensive rats.

Lebrun F L, Lebrun I, Corrêa F M

Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.

Gen Pharmacol. 1994 Jul;25(4):747-52. doi: 10.1016/0306-3623(94)90255-0.

Abstract

We evaluated the involvement of circulating kinins in the hypotensive effect of the antihypertensive drug alpha-methyldopa (alpha-MD) in normotensive rats. 2. The alpha-MD effects were more pronounced in urethane-anesthetized rats than in unanesthetized animals. 3. Treatment with alpha-MD did not affect the circulating levels of kininogen, the bradykinin precursor. 4. Pretreatment with captopril that potentiates the depressor effects of bradykinin did not potentiate the hypotension to alpha-MD. 5. The lack of changes in kininogen levels and the failure of captopril to potentiate the depressor effects of alpha-MD rules out an involvement of the circulating kallikrein-kinin system in the response to alpha-MD.

摘要

我们评估了循环激肽在正常血压大鼠中抗高血压药物α-甲基多巴（α-MD）降压作用中的参与情况。2. α-MD的作用在氨基甲酸乙酯麻醉的大鼠中比在未麻醉的动物中更明显。3. 用α-MD治疗不影响激肽原（缓激肽前体）的循环水平。4. 用卡托普利预处理可增强缓激肽的降压作用，但不能增强对α-MD的低血压作用。5. 激肽原水平缺乏变化以及卡托普利未能增强α-MD的降压作用排除了循环激肽释放酶-激肽系统参与对α-MD反应的可能性。