Jensen L L, Harding J W, Wright J W
Department of Psychology, Washington State University, Pullman 99164.
Am J Physiol. 1992 Jun;262(6 Pt 2):F1068-75. doi: 10.1152/ajprenal.1992.262.6.F1068.
The present investigation examined the abilities of angiotensin (ANG) II and III to produce increases in blood pressure and drinking when microinfused into the paraventricular nucleus (PVN) of the hypothalamus of the Sprague-Dawley rat. Dose-dependent elevations in systemic blood pressure and heart rate were measured to both ANG II and III in the anesthetized rat, with ANG II more potent than ANG III at the two highest doses examined. Pretreatment with the specific ANG receptor antagonist [Sar1,Thr8]ANG II (sarthran), blocked subsequent ANG II- and III-induced elevations in blood pressure, suggesting that these responses were dependent on the activation of ANG receptors. A similar analysis in awake rats yielded nearly equivalent results. A final experiment demonstrated that microinfusions of ANG II and III into the PVN produced drinking in a dose-dependent manner, with greater consumption to ANG II than ANG III. Again, sarthran was found to block the dipsogenic response. Histological examination revealed that the location of the injection site was linked to the character of the ANG-dependent response. These data suggest that the PVN may play a critical role in mediating central ANG effects on body water homeostasis and blood pressure regulation. Furthermore, it appears that subnuclei of the PVN may participate differentially in ANG-mediated actions.
本研究检测了将血管紧张素（ANG）II和III微量注入Sprague-Dawley大鼠下丘脑室旁核（PVN）时，引起血压升高和饮水增加的能力。在麻醉大鼠中，测量了ANG II和III引起的全身血压和心率的剂量依赖性升高，在所检测的两个最高剂量下，ANG II比ANG III更有效。用特异性ANG受体拮抗剂[Sar1，Thr8]ANG II（sarathran）预处理，可阻断随后ANG II和III诱导的血压升高，表明这些反应依赖于ANG受体的激活。在清醒大鼠中进行的类似分析产生了几乎相同的结果。最后一项实验表明，将ANG II和III微量注入PVN会以剂量依赖性方式引起饮水，ANG II引起的饮水量比ANG III更多。同样，发现sarathran可阻断饮水反应。组织学检查显示，注射部位的位置与ANG依赖性反应的特征有关。这些数据表明，PVN可能在介导中枢ANG对机体水平衡和血压调节的作用中起关键作用。此外，PVN的亚核似乎可能以不同方式参与ANG介导的作用。
