Matsumura Y, Hasser E M, Bishop V S
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.
Am J Physiol. 1989 Mar;256(3 Pt 2):R694-700. doi: 10.1152/ajpregu.1989.256.3.R694.
Central effects of angiotensin II (ANG II) on arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) were examined in conscious rabbits. Intravenous infusions of ANG II (5-320 ng.kg-1.min-1) significantly reduced the baroreflex inhibition of HR compared with phenylephrine (PE) (0.5-16 micrograms.kg-1.min-1), whereas reflex inhibition of RSNA was unaltered. Background intravenous infusions of ANG II did not alter the baroreflex responses of RSNA nor HR to increases (with PE) or decreases in mean arterial pressure (with nitroglycerin or inferior vena cava occluder). When ANG II was infused into the vertebral artery (VA) the integrated pressor response was greater than intravenous infusions. Progressive VA infusions of ANG II resulted in a significantly blunted baroreflex inhibition of HR compared with intravenous infusions, whereas the reflex inhibition of RSNA was identical between VA and intravenous infusions. These results suggest that ANG II produces central pressor effects via a hindbrain site and reduces baroreflex inhibition of HR without altering baroreflex inhibition of RSNA.
在清醒家兔中研究了血管紧张素II（ANG II）对肾交感神经活动（RSNA）和心率（HR）的动脉压力反射控制的中枢效应。与去氧肾上腺素（PE）（0.5 - 16微克·千克⁻¹·分钟⁻¹）相比，静脉输注ANG II（5 - 320纳克·千克⁻¹·分钟⁻¹）显著降低了压力反射对HR的抑制作用，而对RSNA的反射性抑制未改变。ANG II的背景静脉输注并未改变RSNA或HR对平均动脉压升高（用PE）或降低（用硝酸甘油或下腔静脉阻断器）的压力反射反应。当将ANG II注入椎动脉（VA）时，综合升压反应大于静脉输注。与静脉输注相比，逐步向VA输注ANG II导致压力反射对HR的抑制作用明显减弱，而VA输注和静脉输注对RSNA的反射性抑制作用相同。这些结果表明，ANG II通过后脑部位产生中枢升压作用，并降低压力反射对HR的抑制作用，而不改变对RSNA的压力反射抑制作用。
