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血管加压素与血管紧张素II在血压和口渴中枢控制中的相互作用。

Interaction of vasopressin and angiotensin II in central control of blood pressure and thirst.

作者信息

Szczepańska-Sadowska E

机构信息

Department of Clinical and Applied Physiology, Warsaw, School of Medicine, Poland.

出版信息

Regul Pept. 1996 Oct 8;66(1-2):65-71. doi: 10.1016/0167-0115(96)00053-5.

Abstract

It is now well recognized that systemically released angiotensin II (Ang II) and arginine vasopressin (AVP) act in concert in regulation of blood pressure and water-electrolyte balance. Numerous studies have also demonstrated that centrally applied Ang II and AVP cause significant alterations of the cardiovascular functions and body fluid balance. Moreover, it has been established that Ang II and AVP are released in the central nervous system during cardiovascular and osmotic disorders and that the cardiovascular regions of the brainstem and the osmoregulatory regions of the forebrain are extensively innervated by the angiotensinergic and vasopressinergic neurons. Some evidence indicates that the angiotensinergic and vasopressinergic system may interact in the central blood pressure control, although the significance of this interaction may differ in various species. Recently, attempts have been made to find out whether centrally released Ang II and AVP may play a role in the regulation of the cardiovascular system under physiological and pathophysiological conditions. With regard to this, the available evidence strongly suggests that the both systems may be involved in regulation of blood pressure under baseline conditions. In addition, the vasopressinergic system appears to be involved in the adjustment of cardiovascular functions to hypovolemia, whereas its role in regulation of blood pressure during the osmotic disorders is less clear. Regulation of blood pressure and heart rate by centrally released AVP under baseline conditions, during hypovolemia and in osmotic disorders is significantly altered in the spontaneously hypertensive rats. It is now well established that centrally applied Ang II and Ang III are potent dipsogenic compounds. There also is evidence that AVP may enhance the osmotic thirst. However, the physiological role of brain-derived AVP and Ang II in the control of water intake awaits further examination. The available evidence from rat studies does not give support to a significant cooperation between central angiotensinergic and vasopressinergic system in regulation of water intake.

摘要

现在人们已经充分认识到,全身释放的血管紧张素II(Ang II)和精氨酸加压素(AVP)共同作用于血压和水电解质平衡的调节。大量研究还表明,中枢给予Ang II和AVP会导致心血管功能和体液平衡发生显著改变。此外,已经确定在心血管和渗透压紊乱期间,Ang II和AVP会在中枢神经系统中释放,并且脑干的心血管区域和前脑的渗透压调节区域广泛地受血管紧张素能神经元和加压素能神经元支配。一些证据表明,血管紧张素能和加压素能系统可能在中枢血压控制中相互作用,尽管这种相互作用的意义在不同物种中可能有所不同。最近,人们试图弄清楚中枢释放的Ang II和AVP在生理和病理生理条件下是否可能在心血管系统的调节中发挥作用。关于这一点,现有证据有力地表明,这两个系统可能在基线条件下参与血压调节。此外,加压素能系统似乎参与心血管功能对血容量减少的调节,而其在渗透压紊乱期间血压调节中的作用尚不清楚。在自发性高血压大鼠中,基线条件下、血容量减少期间和渗透压紊乱时,中枢释放的AVP对血压和心率的调节会发生显著改变。现在已经充分确定,中枢给予的Ang II和Ang III是有效的致渴化合物。也有证据表明AVP可能增强渗透性口渴。然而,脑源性AVP和Ang II在控制水摄入方面的生理作用有待进一步研究。来自大鼠研究的现有证据不支持中枢血管紧张素能和加压素能系统在调节水摄入方面有显著协同作用。

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