Zhu Guo-Qing, Xu Yao, Zhou Li-Min, Li Yue-Hua, Fan Le-Ming, Wang Wei, Gao Xing-Ya, Chen Qi
Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, China.
Exp Physiol. 2009 Jul;94(7):785-94. doi: 10.1113/expphysiol.2008.046565. Epub 2009 Apr 3.
Sympathetic outflow is increased in hypertension. The aim of the present study was to investigate whether the cardiac sympathetic afferent reflex (CSAR) is enhanced in two-kidney one-clip (2K1C) renovascular hypertensive rats, and whether the enhanced CSAR contributes, in part, to the increased sympathetic outflow. Furthermore, the role of central angiotensin II type 1 (AT(1)) receptors in mediating the CSAR was determined. Under urethane and alpha-chloralose anaesthesia, the renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in sinoaortic denervated and cervical vagotomized rats. The CSAR was evaluated by the response of RSNA and MAP to epicardial application of 1.0 nmol of capsaicin. Compared with sham-operated rats, the CSAR, baseline RSNA and plasma noradrenaline level were significantly enhanced in 2K1C rats. Intrapericardial administration of resiniferatoxin, which abolishes the CSAR because of the desensitization of transient receptor potential vanilloid 1-containing cardiac afferent fibres, decreased the RSNA and MAP. The enhanced CSAR in 2K1C rats was normalized by intracerebroventricular administration of the AT(1) receptor antagonist losartan. Intracerebroventricular administration of angiotensin II further potentiated the enhanced CSAR in 2K1C rats, a response which was abolished by pretreatment with losartan. These results indicate that the CSAR is enhanced in 2K1C rats and the enhanced CSAR contributes, in part, to the sympathetic activation and hypertension. Central AT(1) receptors are involved in the enhanced CSAR in 2K1C rats.
高血压患者的交感神经输出增加。本研究的目的是调查在二肾一夹（2K1C）肾血管性高血压大鼠中，心脏交感传入反射（CSAR）是否增强，以及增强的CSAR是否部分促成了交感神经输出的增加。此外，还确定了中枢1型血管紧张素II（AT(1)）受体在介导CSAR中的作用。在乌拉坦和α-氯醛糖麻醉下，记录去窦神经和颈迷走神经切断大鼠的肾交感神经活动（RSNA）和平均动脉压（MAP）。通过RSNA和MAP对心外膜应用1.0 nmol辣椒素的反应来评估CSAR。与假手术大鼠相比，2K1C大鼠的CSAR、基线RSNA和血浆去甲肾上腺素水平显著增强。心包内注射树脂毒素可消除CSAR，因为含瞬时受体电位香草酸亚型1的心脏传入纤维脱敏，从而降低了RSNA和MAP。脑室注射AT(1)受体拮抗剂氯沙坦可使2K1C大鼠增强的CSAR恢复正常。脑室注射血管紧张素II进一步增强了2K1C大鼠增强的CSAR，氯沙坦预处理可消除这一反应。这些结果表明，2K1C大鼠的CSAR增强，且增强的CSAR部分促成了交感神经激活和高血压。中枢AT(1)受体参与了2K1C大鼠CSAR的增强。
