Cowley A W
Department of Physiology, Medical College of Wisconsin, Milwaukee.
Clin Physiol Biochem. 1988;6(3-4):150-62.
The vasoconstrictor actions of arginine vasopressin (AVP) have been shown to occur in concentrations much lower than previously thought. Pressor responses to AVP are a poor index of vasoconstrictor activity since, in contrast to other vasoconstrictor agents, the expected rise of pressure is offset by dose-dependent decreases of cardiac output. The mechanisms for this appear to be, in large part, modulation of the autonomic nervous system whereby AVP enhances vagal nerve activity and reduces peripheral sympathetic nerve activity. AVP enhancement of baroreceptor reflex gain is in part responsible for these changes in some species (dog and rabbit), but not in others (rat). The release of AVP appears to contribute significantly to the normalization of arterial pressure in volume-depleted and hypotensive states. The link between plasma AVP and hypertension remains unclear, but it appears likely that it has an important permissive action in the development of sodium-dependent forms of hypertension.
精氨酸加压素(AVP)的血管收缩作用已被证明在比之前认为的浓度低得多的情况下就会发生。对AVP的升压反应并不是血管收缩活性的良好指标,因为与其他血管收缩剂不同,预期的血压升高会被心输出量的剂量依赖性降低所抵消。其机制在很大程度上似乎是自主神经系统的调节,即AVP增强迷走神经活动并降低外周交感神经活动。在某些物种(狗和兔子)中,AVP增强压力感受器反射增益在一定程度上导致了这些变化,但在其他物种(大鼠)中并非如此。在血容量减少和低血压状态下,AVP的释放似乎对动脉血压的正常化有显著贡献。血浆AVP与高血压之间的联系仍不清楚,但在钠依赖性高血压的发展中,它似乎可能具有重要的允许作用。