Rascher W
Klin Wochenschr. 1985 Oct 1;63(19):989-99. doi: 10.1007/BF01737635.
The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.
血管加压素的两个主要生物学作用是抗利尿和血管收缩。低浓度血管加压素的抗利尿作用已得到充分证实,抗利尿所需浓度10至100倍以上的血管加压素会升高动脉血压。抗利尿作用由肾脏的V2受体介导,而血管加压素通过与V1受体结合使小动脉收缩。本文介绍了血管加压素血管收缩活性特异性拮抗剂(血管或V1受体拮抗剂)的药理作用。低浓度的血管加压素确实具有显著的血流动力学效应。生理浓度的血管加压素会引起血管收缩并升高全身血管阻力。然而,在心血管反射活动正常的受试者中,心输出量会随之下降,因此血压不会改变。在压力感受器去传入的动物或压力感受器反射迟钝(自主神经功能不全)的患者中,血浆血管加压素升高会导致血管收缩和血压升高,因为在这些情况下心输出量不会下降。在禁水期间,血管加压素通过增加全身血管阻力对维持血压有重要作用。在出血和低血压期间,血管加压素在恢复血压方面起主要作用。在实验性高血压中,血管加压素在去氧皮质酮(DOCA)诱导的高血压的发生和维持中起作用,但在遗传性高血压大鼠中不起作用。血管加压素在人类高血压中的作用尚不清楚。脑下丘脑外区域的血管加压素通过与中枢心血管控制中心相互作用影响循环调节。血管加压素如何参与血压中枢调节的确切机制仍有待确定。与我们之前的观点相反,血管加压素在低血浆浓度时也是一种血管活性激素。其心血管作用比之前认为的更为复杂。