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

机译:血管加压素和血管紧张素II的相互作用可控制血压和口渴。

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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.
机译:现在已经众所周知,全身释放的血管紧张素II(Ang II)和精氨酸加压素(AVP)在调节血压和水电解质平衡中起着协同作用。大量研究还表明,集中应用Ang II和AVP会引起心血管功能和体液平衡的显着改变。此外,已经确定在心血管和渗透性疾病期间Ang II和AVP在中枢神经系统中释放,并且脑血管的区域和前脑的渗透调节区域被血管紧张素能和血管加压素能神经元广泛支配。一些证据表明,血管紧张素能和血管加压素能系统可能在中央血压控制中相互作用,尽管这种相互作用的重要性在不同物种中可能有所不同。最近,已经尝试找出在生理和病理生理条件下中枢释放的Ang II和AVP是否可能在心血管系统的调节中起作用。关于这一点,现有证据有力地表明,这两种系统都可能参与基线条件下的血压调节。另外,血管加压素系统似乎参与了对低血容量的心血管功能的调节,而在渗透性疾病期间其在血压调节中的作用尚不清楚。自发性高血压大鼠在基线状态下,血容量不足和渗透性疾病中通过中央释放的AVP对血压和心率的调节显着改变。现在已经很好地确定,集中施用的Ang II和Ang III是有效的浸源化合物。也有证据表明AVP可以增强渗透性口渴。然而,脑源性AVP和Ang II在控制饮水中的生理作用有待进一步研究。来自大鼠研究的现有证据并未支持中央血管紧张素能和血管加压素能系统在调节饮水量方面的重要合作。

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