Hatzinikolaou P, Gavras H, Brunner H R, Gavras I
Am J Physiol. 1981 Jun;240(6):H827-31. doi: 10.1152/ajpheart.1981.240.6.H827.
Elevation of blood pressure induced by an acute sodium and fluid load in the anephric state has been attributed to intravascular fluid volume expansion. The present experiments were designed to study the role of vasopressin and catecholamines in this type of hypertension. Normotensive anephric rats, adrenergically intact or pretreated with alpha- and beta-adrenoceptor blockade, and deoxycorticosterone (DOC)-salt-treated anephric rats, intact or pretreated with alpha- and beta-adrenoceptor blockade, received an infusion of 2 ml containing 3 meq NaCl, followed by intravenous administration of an analogue antagonist of the vasopressor effect of arginine-vasopressin (AVP). Pressure increments induced by hypertonic saline were abolished by an AVP antagonist partly in the adrenergically intact animals (leaving a small residual pressure elevation) and completely in adrenergically blocked animals, which had a larger AVP component. Volumes expansion did not necessarily accompany increase in blood pressure after saline infusion. In fact some DOC-salt-treated animals with the highest blood pressures and norepinephrine levels exhibited contraction of plasma volume. Increments in blood pressure were negatively correlated with plasma volume changes (r = -0.687, P less than 0.05) in these animals and positively with norepinephrine levels in all adrenergically intact animals (r = 0.818, P less than 0.001). It is concluded that the hypertensive response elicited by acute hypertonic saline load is due to vasoconstriction mediated partly by vasopressin and partly by the sympathetic system, which may in some way attenuate the effect of vasopressin.
在无肾状态下，急性钠和液体负荷引起的血压升高被归因于血管内容量扩张。本实验旨在研究血管加压素和儿茶酚胺在这类高血压中的作用。血压正常的无肾大鼠，肾上腺能功能正常或用α和β肾上腺素能受体阻滞剂预处理，以及用脱氧皮质酮（DOC）-盐处理的无肾大鼠，肾上腺能功能正常或用α和β肾上腺素能受体阻滞剂预处理，接受2毫升含3毫当量氯化钠的输注，随后静脉注射精氨酸血管加压素（AVP）升压作用的类似物拮抗剂。在肾上腺能功能正常的动物中，AVP拮抗剂部分消除了高渗盐水引起的压力升高（留下小的残余压力升高），而在肾上腺能功能被阻断的动物中则完全消除，这些动物的AVP成分更大。盐水输注后，容量扩张不一定伴随着血压升高。事实上，一些血压和去甲肾上腺素水平最高的DOC-盐处理动物表现出血浆容量收缩。在这些动物中，血压升高与血浆容量变化呈负相关（r = -0.687，P < 0.05），而在所有肾上腺能功能正常的动物中与去甲肾上腺素水平呈正相关（r = 0.818，P < 0.001）。得出的结论是，急性高渗盐水负荷引起的高血压反应是由于血管收缩，部分由血管加压素介导，部分由交感神经系统介导，交感神经系统可能以某种方式减弱血管加压素的作用。
