A novel effect of angiotensin on renal sympathetic nerve activity in mice
A novel effect of angiotensin on renal sympathetic nerve activity in mice
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DOI：
10.1097/00004872-200103001-00014
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发表时间：
2001-03-01
影响因子：
4.9
通讯作者：
Chapleau, MW
中科院分区：
文献类型：
--
作者：
Ma, XY;Abboud, FM;Chapleau, MW
目的观察血管紧张素Ⅱ（angiotensin Ⅱ，Ang Ⅱ）对小鼠肾交感神经活动（renal sympathetic nerve activity，RSNA）的影响，并探讨其作用机制。给予Ang II（4 ng/g）增加动脉压并诱发RSNA的双相变化：抑制继发于动脉压初始升高的RSNA的高振幅相位爆发，随后激活超过基线活性的低振幅连续放电RSNA（255 +/-72%基线，n = 8）。平均动脉压（MAP）的峰值变化为+60 +/- 4 mmHg（n = 8）。在同一组动物中，去甲肾上腺素（40 ng/g）引起MAP（+57 +/- 5 mmHg）等效增加，并基本消除RSNA。Ang II诱导的RSNA激活呈剂量依赖性（0.5-4 ng/g，n = 7），并可被Ang II 1型（AT（1））受体阻断剂氯沙坦（10 μ g/g，i. v.）(301+/- 61 vs 117 +/- 22%基线，氯沙坦之前vs之后，n = 5），神经节阻滞剂，六甲铵（30 μ g/g，静脉注射），消除了基线高幅度的RSNA爆发，但没有钝化Ang II诱导的RSNA（n = 6）。结论Ang Ⅱ激活肾交感神经，其机制可能与ATI受体介导的节后交感神经元的直接激活有关。
Objective The goals of this study were to characterize the effects of angiotensin II (Ang II) on renal sympathetic nerve activity (RSNA) and to define mechanisms of its actions in mice.Design The experiments were performed in sodium pentobarbital anesthetized C57BL/6J mice to investigate the effects of intravenous administration of Ang II on RSNA recorded from renal sympathetic post-ganglionic nerve fibers.Results Intravenous (i.v.) administration of Ang II (4 ng/g) increased arterial pressure and evoked a biphasic change in RSNA: inhibition of high-amplitude phasic bursts of RSNA secondary to the initial rise of arterial pressure followed by activation of low-amplitude continuously discharging RSNA that exceeded baseline activity (255 +/- 72% baseline, n = 8). The peak change of mean arterial pressure (MAP) was +60 +/- 4 mmHg (n = 8). In the same group of animals, norepinephrine (40 ng/g) caused an equivalent increase in MAP (+57 +/- 5 mmHg) and essentially abolished RSNA. The Ang Ii-induced activation of RSNA was dose-dependent (0.5-4 ng/g, n = 7) and was abolished by the Ang II type 1 (AT(1)) receptor blocker, losartan (10 mug/g, i.v.)(301 +/- 61 versus 117 +/- 22% baseline, before versus after losartan, n = 5), The ganglionic blocker, hexamethonium (30 mug/g, i.v.), eliminated baseline high-amplitude bursts of RSNA but did not blunt the Ang Ii-induced RSNA (n = 6). In baroreceptor denervated and vagotomized mice, Ang II failed to inhibit high-amplitude bursts of RSNA but continued to trigger low-amplitude continuous RSNA.Conclusion We conclude that Ang II activates renal sympathetic nerves that discharge in a continuous pattern, distinctly different than the normal baseline high-amplitude bursts of RSNA, The mechanism may involve direct activation of post-ganglionic sympathetic neurons mediated through ATI receptors.