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绵羊醛固酮分泌的中枢多巴胺能调节

Central dopaminergic regulation of aldosterone secretion in sheep.

作者信息

Huang B S, Malvin R L, Lee J, Grekin R J

出版信息

Hypertension. 1987 Aug;10(2):157-63. doi: 10.1161/01.hyp.10.2.157.

Abstract

Central dopaminergic mechanisms involved in the regulation of plasma aldosterone concentration were investigated in 16 conscious sheep following Na depletion with intramuscularly administered furosemide. Intracerebroventricular infusion of dopamine (20 micrograms/min) decreased plasma aldosterone significantly to 52 +/- 8% of basal level and increased plasma renin activity (PRA) significantly to 172 +/- 25% of basal level in this animal model. In addition, intracerebroventricular infusion of the dopamine antagonist metoclopramide (20 micrograms/min) in artificial cerebrospinal fluid vehicle significantly increased aldosterone levels to 144 +/- 14% of basal level and decreased PRA to 62 +/- 5% of basal value. Neither intracerebroventricular infusion of the vehicle nor intravenous infusions of metoclopramide or dopamine at the same doses changed aldosterone or PRA levels. Intracerebroventricular bolus injections of metoclopramide (20 micrograms/kg in 0.4 ml of vehicle) were also effective, increasing aldosterone levels to 266 +/- 22% of basal level and decreasing PRA to 70 +/- 12% of basal level. Intravenous bolus injections of the same dose of metoclopramide were ineffective. Dopamine was infused intracerebroventricularly into two uniadrenalectomized sheep with the remaining adrenal transplanted to the neck. Aldosterone levels were decreased to 49 +/- 10% of basal level, and PRA was increased to 157 +/- 10% of basal value. None of the infusions or injections changed arterial or intracranial pressure, or plasma K, Na, and cortisol levels. These data indicate that endogenous or exogenous dopamine may act on central dopamine receptors to decrease plasma aldosterone concentration by an unknown humoral mechanism. The known aldosterone regulators, plasma Na, K, angiotensin II, and adrenocorticotropic hormone, are not involved in the regulation.

摘要

在16只经肌肉注射速尿造成钠缺失的清醒绵羊中,研究了参与调节血浆醛固酮浓度的中枢多巴胺能机制。在该动物模型中,脑室内输注多巴胺(20微克/分钟)可使血浆醛固酮显著降低至基础水平的52±8%,并使血浆肾素活性(PRA)显著升高至基础水平的172±25%。此外,在人工脑脊液载体中脑室内输注多巴胺拮抗剂甲氧氯普胺(20微克/分钟)可使醛固酮水平显著升高至基础水平的144±14%,并使PRA降低至基础值的62±5%。脑室内输注载体以及静脉输注相同剂量的甲氧氯普胺或多巴胺均未改变醛固酮或PRA水平。脑室内推注甲氧氯普胺(20微克/千克,溶于0.4毫升载体中)也有效,可使醛固酮水平升高至基础水平的266±22%,并使PRA降低至基础水平的70±12%。静脉推注相同剂量的甲氧氯普胺则无效。将多巴胺脑室内输注到两只单侧肾上腺切除且将剩余肾上腺移植到颈部的绵羊体内。醛固酮水平降低至基础水平的49±10%,PRA升高至基础值的157±10%。所有输注或注射均未改变动脉压或颅内压,也未改变血浆钾、钠和皮质醇水平。这些数据表明,内源性或外源性多巴胺可能通过未知的体液机制作用于中枢多巴胺受体,从而降低血浆醛固酮浓度。已知的醛固酮调节因子,如血浆钠、钾、血管紧张素II和促肾上腺皮质激素,均未参与该调节过程。

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