O'Neill T P, Brody M J
Am J Physiol. 1987 Jun;252(6 Pt 2):R1165-72. doi: 10.1152/ajpregu.1987.252.6.R1165.
Recent evidence suggests an important role for the median preoptic nucleus (MnPO) in cardiovascular responses evoked by angiotension II (ANG II). We therefore planned to determine whether selective inactivation of this nucleus would produce deficits in pressor responsiveness to centrally administered ANG II and carbachol. Chronic disruption of MnPO by electrolytic lesion produced pressor deficits to centrally administered ANG II and carbachol but did not change resting arterial pressure. In addition, blockade of neuronal activity in MnPO produced by the microinjection of the local anesthetic lidocaine reversibly attenuated pressor responses to these agents without producing any change in resting arterial pressure. The microinjection of ANG II itself into sites in which lidocaine blocked ANG II pressor responses had no effect on arterial pressure but did produce drinking. These data suggest that the MnPO, although not acting as a receptor site for the pressor effect of ANG II, plays an important role in mediating the pressor response evoked by centrally administered ANG II and carbachol.
最近的证据表明，视前正中核（MnPO）在血管紧张素II（ANG II）引发的心血管反应中起重要作用。因此，我们计划确定该核团的选择性失活是否会导致对中枢给予的ANG II和卡巴胆碱的升压反应性出现缺陷。通过电解损伤对MnPO进行慢性破坏会导致对中枢给予的ANG II和卡巴胆碱的升压缺陷，但不会改变静息动脉血压。此外，通过微量注射局部麻醉药利多卡因对MnPO中的神经元活动进行阻断，可可逆地减弱对这些药物的升压反应，而不会使静息动脉血压发生任何变化。将ANG II自身微量注射到利多卡因阻断ANG II升压反应的部位对动脉血压没有影响，但会引起饮水。这些数据表明，MnPO虽然不是ANG II升压作用的受体部位，但在介导中枢给予的ANG II和卡巴胆碱引发的升压反应中起重要作用。
