Sasaki S, Dampney R A
Department of Physiology, University of Sydney, Australia.
Hypertension. 1990 Mar;15(3):274-83. doi: 10.1161/01.hyp.15.3.274.
The rostral and caudal parts of the ventrolateral medulla play a major role in the control of blood pressure. Both regions contain a high density of receptor binding sites for angiotensin II, and it has been shown previously that microinjection of angiotensin II into the rostral ventrolateral medulla causes a rise in blood pressure. The aims of this study were to determine the cardiovascular effects of microinjection of angiotensin II and its specific antagonist [Sar1Thr8]angiotensin II into the caudal ventrolateral medulla and to characterize the regional vascular effects elicited by both compounds in the rostral ventrolateral medulla. Microinjections of angiotensin II (0.2-20 pmol) into histologically verified sites in the caudal ventrolateral medulla of anesthetized baroreceptor-denervated rabbits produced dose-dependent decreases in blood pressure and renal sympathetic nerve activity, whereas microinjection of [Sar1Thr8]angiotensin II (40 pmol) produced increases in these variables. In the rostral ventrolateral medulla, angiotensin II (0.02-20 pmol) elicited a dose-dependent increase in blood pressure, iliac vascular resistance, and renal sympathetic nerve activity, whereas [Sar1Thr8]angiotensin II (40 pmol) produced decreases in these variables. The effects on heart rate elicited by either compound in the rostral or caudal ventrolateral medulla were small but were in the same direction as the other cardiovascular variables. In contrast, angiotensin II had no detectable effect on sympathoexcitatory neurons within the rostral dorsomedial medulla, a region that lacks angiotensin II receptor binding sites. The results indicate that endogenous angiotensin II acts on specific receptors within the rostral and caudal parts of the ventrolateral medulla and has a tonic excitatory action on sympathoexcitatory and sympathoinhibitory neurons within these respective regions.
延髓腹外侧的头端和尾端部分在血压控制中起主要作用。这两个区域都含有高密度的血管紧张素II受体结合位点，并且先前已经表明，向延髓腹外侧头端微量注射血管紧张素II会导致血压升高。本研究的目的是确定向延髓腹外侧尾端微量注射血管紧张素II及其特异性拮抗剂[Sar1Thr8]血管紧张素II的心血管效应，并描述这两种化合物在延髓腹外侧头端引起的局部血管效应。向麻醉的、压力感受器去神经的家兔延髓腹外侧尾端经组织学验证的部位微量注射血管紧张素II（0.2 - 20皮摩尔）会使血压和肾交感神经活动呈剂量依赖性降低，而微量注射[Sar1Thr8]血管紧张素II（40皮摩尔）会使这些变量增加。在延髓腹外侧头端，血管紧张素II（0.02 - 20皮摩尔）会引起血压、髂血管阻力和肾交感神经活动呈剂量依赖性增加，而[Sar1Thr8]血管紧张素II（40皮摩尔）会使这些变量降低。这两种化合物在延髓腹外侧头端或尾端对心率的影响较小，但与其他心血管变量的变化方向相同。相比之下，血管紧张素II对延髓背内侧头端内的交感兴奋性神经元没有可检测到的作用，该区域缺乏血管紧张素II受体结合位点。结果表明，内源性血管紧张素II作用于延髓腹外侧头端和尾端的特定受体，并对这些相应区域内的交感兴奋性和交感抑制性神经元具有紧张性兴奋作用。
