Mangiapane M L, Simpson J B
Am J Physiol. 1980 Nov;239(5):R382-9. doi: 10.1152/ajpregu.1980.239.5.R382.
Intracranial injection of angiotensin II (AII) at three brain sites elicited near simultaneous dipsogenic and pressor effects in rats. Both effects were maximal, occurred with the shortest latencies, and at the lowest doses of AII when the cannula terminated precisely within the parenchyma of the subfornical organ (SFO). Pressor effects were produced by SFO injection of a dose of AII (0.1 pg) which approximates plasma AII concentrations at the high end of the physiological range. Both the drinking and pressor effects were blocked by saralasin. Injections of AII at sites immediately adjacent to SFO produced smaller effects with longer latencies. These results ruled out the possibility that SFO injections were effective via leakage to alternative sites. The pressor effect of AII at the SFO remained in animals under chloralose anesthesia, demonstrating that it is not an artifact of drinking behavior. These results indicate that the SFO is a site of AII pressor action, and confirm previous demonstrations that the structure is a site of AII drinking action.
在大鼠的三个脑区进行颅内注射血管紧张素II（AII），可引发几乎同时出现的致渴和升压效应。当套管精确终止于穹窿下器（SFO）实质内时，这两种效应均达到最大，潜伏期最短，且所需的AII剂量最低。在SFO注射一剂接近生理范围高端血浆AII浓度的AII（0.1皮克）可产生升压效应。饮水和升压效应均被沙拉新阻断。在紧邻SFO的部位注射AII产生的效应较小，潜伏期较长。这些结果排除了SFO注射通过渗漏至其他部位而产生效应的可能性。在氯醛糖麻醉的动物中，AII在SFO的升压效应依然存在，表明这并非饮水行为的假象。这些结果表明，SFO是AII升压作用的部位，并证实了先前的研究结果，即该结构是AII引发饮水行为的部位。
