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犬体内内源性阿片类物质拮抗作用对肾素释放的抑制

Suppression of renin release by antagonism of endogenous opiates in the dog.

作者信息

Szilagyi J E, Chelly J, Doursout M F

出版信息

Am J Physiol. 1986 Apr;250(4 Pt 2):R633-7. doi: 10.1152/ajpregu.1986.250.4.R633.

Abstract

The influence of blockade of endogenous opioids on the release of renin due to partial renal arterial constriction was determined acutely and chronically in unilaterally nephrectomized dogs. In acute preparations changes in plasma renin activity, arterial blood pressure, and heart rate were determined after 15 min of 60% renal arterial constriction before and after administration of either a saline vehicle, the opiate antagonist naloxone (0.05 mg/kg), or morphine (2 mg/kg). Acute antagonism of endogenous opiates abolished the increase in plasma renin activity and mean arterial pressure associated with renal arterial constriction. Repeated renal arterial constrictions in saline- or morphine-treated animals did not alter the humoral or hemodynamic responses. In chronic preparations long-term naloxone infusion attenuated the development of renovascular hypertension and diminished the increase in plasma renin activity. These data suggest that endogenous opioid peptides are modulators in the control of renin release and may be important participants in the pathogenesis of hypertension.

摘要

在单侧肾切除的犬中,急性和慢性地测定了内源性阿片类物质阻断对部分肾动脉狭窄所致肾素释放的影响。在急性实验中,在给予生理盐水载体、阿片拮抗剂纳洛酮(0.05mg/kg)或吗啡(2mg/kg)之前和之后,对肾动脉进行60%狭窄15分钟后,测定血浆肾素活性、动脉血压和心率的变化。内源性阿片类物质的急性拮抗作用消除了与肾动脉狭窄相关的血浆肾素活性和平均动脉压的升高。在生理盐水或吗啡处理的动物中反复进行肾动脉狭窄,并未改变体液或血流动力学反应。在慢性实验中,长期输注纳洛酮可减轻肾血管性高血压的发展,并减少血浆肾素活性的升高。这些数据表明,内源性阿片肽是肾素释放控制中的调节因子,可能是高血压发病机制中的重要参与者。

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