Casto R, Phillips M I
Am J Physiol. 1984 Sep;247(3 Pt 2):R575-81. doi: 10.1152/ajpregu.1984.247.3.R575.
We recently reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) results in an increase in mean arterial pressure (MAP) in urethan-anesthetized rats in a dose range of 50-500 ng. To investigate the mechanism of this response, hexamethonium (20 mg/kg iv) was used to inhibit sympathetic activation. There was a highly significant (P less than 0.001) reduction in the magnitude of the pressor response (4.7 +/- 1.1 mmHg) compared with preblockade ANG II (500 ng) responses (15.5 +/- 1.6 mmHg). A vasopressin antagonist and hypophysectomized rats were used to study the contribution of pituitary vasopressin. Injection of 500 ng ANG II in hypophysectomized rats produced a pressor response (14.8 +/- 3.2 mmHg) indistinguishable from that in intact controls (15.5 +/- 1.6 mmHg). Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)AVP (1 microgram iv) in intact rats also had no effect on the magnitude of the pressor response (15.7 +/- 1.7 mmHg). Microinjection of ANG I and II produces an increase in arterial pressure. It is concluded that the angiotensin pressor response in the NTS is mediated by activation of descending sympathetic fibers and is not dependent on release of blood-borne pressor agents from the pituitary.
我们最近报道，向孤束核（NTS）微量注射血管紧张素II（ANG II）可使乌拉坦麻醉大鼠的平均动脉压（MAP）在50 - 500 ng的剂量范围内升高。为研究这种反应的机制，使用六甲铵（20 mg/kg静脉注射）抑制交感神经激活。与阻断前ANG II（500 ng）反应（15.5±1.6 mmHg）相比，升压反应幅度（4.7±1.1 mmHg）有极显著降低（P小于0.001）。使用血管加压素拮抗剂和垂体切除的大鼠来研究垂体血管加压素的作用。向垂体切除的大鼠注射500 ng ANG II产生的升压反应（14.8±3.2 mmHg）与完整对照大鼠（15.5±1.6 mmHg）无差异。在完整大鼠中预先用血管加压素拮抗剂d(CH2)5Tyr(Me)AVP（1 μg静脉注射）处理，对升压反应幅度（15.7±1.7 mmHg）也无影响。微量注射ANG I和II可使动脉压升高。结论是，NTS中的血管紧张素升压反应是由下行交感神经纤维的激活介导的，不依赖于垂体释放的血源性升压物质。
