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[甲状旁腺激素对正常血压和自发性高血压大鼠心血管系统对血管紧张素-2反应性的影响]

[The effect of parathormone on the reactivity of the cardiovascular system to angiotensin-2 in normotensive and spontaneously hypertensive rats].

作者信息

Brin V B, Tatrov A S

出版信息

Fiziol Zh SSSR Im I M Sechenova. 1990 Mar;76(3):345-50.

PMID:2164967
Abstract

The effect of parathyroid hormone (2 units/100 g) on hemodynamic response to various doses of i.v. angiotensin-2 (16 ng/100 g; 20 ng/100 g; 24 ng/100 g) was studied in normotensive and spontaneously hypertensive rats. The effect involved a decrease of the minute blood volume, stroke volume, and an increase of total peripheral resistance in normotensive rats. Parathyroid hormone decreased total peripheral resistance and increased the minute blood volume and the heart rate in spontaneously hypertensive rats. Angiotensin-2 raised the arterial pressure in normotensive rats. In presence of parathyroid hormone, the angiotensin-2 pressor effect was quite obvious in normotensive rats whereas in spontaneously hypertensive rats angiotensin-2 effect caused the greatest rise of arterial pressure as a result of a considerable dose-dependent rise of total peripheral resistance, the cardiac output showing a tendency towards a reduction.

摘要

在正常血压和自发性高血压大鼠中,研究了甲状旁腺激素(2单位/100克)对不同剂量静脉注射血管紧张素-2(16纳克/100克;20纳克/100克;24纳克/100克)血液动力学反应的影响。该影响包括正常血压大鼠的每分钟血容量、每搏输出量降低,以及总外周阻力增加。甲状旁腺激素降低了自发性高血压大鼠的总外周阻力,增加了每分钟血容量和心率。血管紧张素-2使正常血压大鼠的动脉压升高。在存在甲状旁腺激素的情况下,血管紧张素-2的升压作用在正常血压大鼠中相当明显,而在自发性高血压大鼠中,血管紧张素-2的作用导致动脉压最大程度升高,这是由于总外周阻力显著的剂量依赖性升高,心输出量呈现减少趋势。

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