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抗利尿激素释放中的中枢胆碱能和肾上腺素能机制。

Central cholinergic and adrenergic mechanisms in the release of antidiuretic hormone.

作者信息

Bhargava K P, Kulshrestha V K, Srivastava Y P

出版信息

Br J Pharmacol. 1972 Apr;44(4):617-27. doi: 10.1111/j.1476-5381.1972.tb07301.x.

Abstract
  1. Studies on the urine outflow, blood ADH concentration and electrolyte excretion were carried out in alpha-chloralose anaesthetized hydrated dogs; the agonists and antagonists of specific cholinoceptors and adrenoceptors were injected by the intracerebroventricular technique, to delineate the role of the C.N.S. receptors in the control of ADH secretion.2. Central injection of acetylcholine elicited a dose-dependent antidiuretic response which was associated with an increase in the blood ADH titre. Central atropinization partially blocked the antidiuretic response. The remaining antidiuretic response was reversed to a diuretic one by further pretreatment with phenoxybenzamine. The diuretic response thus obtained could be blocked by propranolol.3. The alpha-adrenoceptor agonists, phenylephrine and noradrenaline, induced dose-dependent antidiuretic responses with a concomitant rise in blood ADH concentration. Their effect could be blocked by pretreatment centrally with phenoxybenzamine. Low doses of adrenaline induced a diuretic response and a decrease in blood ADH concentration, higher doses elicited a dose-dependent antidiuretic response and increase in the titre of ADH in blood. Central phenoxybenzamine pretreatment reversed the antidiuretic effect of high doses of adrenaline to a diuretic effect which could be blocked by propranolol.4. Isoprenaline elicited a dose-dependent diuretic response and a decrease in blood ADH titre and propranolol competitively blocked the effect of isoprenaline.5. It is concluded that central muscarinic cholinoceptors and the alpha-adrenoceptors are concerned in the release of ADH, whereas the beta-adrenoceptors are concerned with inhibition of ADH release.
摘要
  1. 对用α-氯醛糖麻醉并补充水分的犬进行了尿液排出、血液抗利尿激素(ADH)浓度及电解质排泄的研究;采用脑室内注射技术注入特异性胆碱能受体和肾上腺素能受体的激动剂和拮抗剂,以阐明中枢神经系统(C.N.S.)受体在控制ADH分泌中的作用。

  2. 脑室内注射乙酰胆碱引发剂量依赖性抗利尿反应,这与血液中ADH水平升高有关。中枢给予阿托品可部分阻断抗利尿反应。剩余的抗利尿反应在用苯氧苄胺进一步预处理后转变为利尿反应。如此获得的利尿反应可被普萘洛尔阻断。

  3. α-肾上腺素能受体激动剂去氧肾上腺素和去甲肾上腺素诱导剂量依赖性抗利尿反应,同时血液中ADH浓度升高。其作用可通过中枢给予苯氧苄胺预处理来阻断。低剂量肾上腺素诱导利尿反应并使血液中ADH浓度降低,高剂量则引发剂量依赖性抗利尿反应并使血液中ADH水平升高。中枢给予苯氧苄胺预处理可将高剂量肾上腺素的抗利尿作用转变为利尿作用,该利尿作用可被普萘洛尔阻断。

  4. 异丙肾上腺素引发剂量依赖性利尿反应并使血液中ADH水平降低,普萘洛尔可竞争性阻断异丙肾上腺素的作用。

  5. 得出的结论是,中枢毒蕈碱胆碱能受体和α-肾上腺素能受体与ADH的释放有关,而β-肾上腺素能受体与ADH释放的抑制有关。

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