Ota K, Kimura T, Inoue M, Funyu T, Shoji M, Sato K, Ohta M, Yamamoto T, Abe K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Eur J Endocrinol. 1995 Jul;133(1):127-32. doi: 10.1530/eje.0.1330127.
To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with non-peptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release.
为研究血管加压素（AVP）受体在调节血流动力学及心房利钠肽（ANP）释放中的作用，以及肾神经传入在渗透性AVP释放中的参与情况，将高渗盐水（HS）注入清醒、双侧肾切除且使用AVP V1受体或V2受体非肽类选择性拮抗剂的大鼠体内。对照组中，单独使用HS可使平均动脉压、血浆ANP和AVP、血浆容量及血浆渗透压升高，并使心率降低。在V1受体拮抗剂组，平均动脉压升高及心率降低被完全消除，血浆ANP升高减弱。在V2受体拮抗剂组，平均动脉压和血浆ANP升高及心率降低减弱。然而，V2受体拮抗剂组中心率变化与平均动脉压变化的比值显著高于对照组。在两个实验组中，血浆AVP、血浆容量及血浆渗透压的升高与对照组无差异。这些结果表明，HS诱导的平均动脉压升高主要通过V1受体由AVP的升压作用介导，且AVP通过V2受体的降压作用可能不会影响HS持续诱导的高血压。此外，HS诱导的血浆ANP升高主要由血浆容量和血压升高介导，但可能不受AVP对心脏的直接作用影响。肾传入神经输入可能对渗透性AVP释放的调节无作用。
