Robertson G L, Ganguly A
J Cardiovasc Pharmacol. 1986;8 Suppl 7:S87-91. doi: 10.1097/00005344-198600087-00017.
Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
血管升压素的分泌受高渗、血容量减少或低血压刺激，受低渗、血容量增加或高血压抑制。这些渗透压和血流动力学影响由起源于不同渗透压感受器或压力感受器的神经传入介导，但最终汇聚作用于相同的神经分泌神经元。在功能上，这两个控制系统以这样一种方式整合，即渗透压调节会改变但不会被血流动力学影响破坏。在无并发症的原发性高血压患者中，基础血管升压素以及渗透压刺激的血管升压素完全正常。如果将数值相对于压力变化来表示，血管升压素对急性血压降低的反应也正常。然而，如果将血浆血管升压素反应绘制为绝对血压的函数，描述这种关系的曲线位于正常曲线的右侧。因此，尽管压力调节机制完全正常，但在原发性高血压中它似乎被重置到了更高水平。这些结果表明，血管升压素分泌增加对无并发症、未经治疗的原发性高血压的发生或维持没有作用，但可能会拮抗某些抗高血压药物的治疗效果。如果是这样，V1受体拮抗剂可能作为这种情况的二线辅助治疗药物有用。
