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压力感受器激活或谷氨酸共注射促进了向孤束核微量注射心钠素时的降压反应。

Baroreceptor activation or glutamate coinjection facilitates depressor responses to ANF microinjection into NTS.

作者信息

McKitrick D J, Calaresu F R

机构信息

Department of Physiology, University of Western Ontario, London, Canada.

出版信息

Am J Physiol. 1989 Aug;257(2 Pt 2):R405-9. doi: 10.1152/ajpregu.1989.257.2.R405.

Abstract

As microinjection of atrial natriuretic factor (ANF) into the nucleus of the solitary tract (NTS) has been shown to elicit depressor responses [D. J. McKitrick and F. R. Calaresu. Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R182-R187, 1988], we investigated the possibility that these responses might be facilitated either by electrical stimulation of arterial baroreceptor fibers in the aortic depressor nerve (ADN) or by simultaneous microinjection of L-glutamate (Glu) into the same sites in the NTS. Male Wistar rats (n = 51) were anesthetized with urethan (1.4 g/kg ip), artificially ventilated, and the dorsal medulla was exposed. The ADN was isolated, cut distally, and the central end was placed on bipolar stimulating electrodes. Threshold doses of 10(-7) M ANF microinjected into the NTS were combined with threshold electrical stimulation of the ADN (n = 37) or threshold doses of 0.13-0.5 M Glu (n = 14) microinjected into the NTS. There was a significant interaction between ANF microinjection and ADN stimulation in producing changes in mean arterial pressure (MAP) and heart rate [HR; P less than 0.05; -20.2 +/- 2.3 (SE) mmHg and -30.8 +/- 6.9 (SE) beats/min, respectively; n = 18]. There was also a significant interaction between ANF and Glu in producing changes in MAP and HR [P less than 0.05; -16.3 +/- 1.8 (SE) mmHg and -15.0 +/- 3.0 (SE) beats/min, respectively; n = 8]. These results indicate that ANF influences neurons in the NTS, which are also influenced by activation of arterial baroreceptors, and ANF and Glu interact in the NTS to produce facilitated cardiovascular responses.

摘要

由于已证明将心房利钠因子(ANF)微量注射到孤束核(NTS)中会引发降压反应[D. J. 麦基特里克和F. R. 卡莱雷苏。《美国生理学杂志》255卷(调节整合生理学24):R182 - R187,1988年],我们研究了以下可能性:这些反应可能通过电刺激主动脉减压神经(ADN)中的动脉压力感受器纤维,或者通过同时将L - 谷氨酸(Glu)微量注射到NTS中的相同部位而得到增强。雄性Wistar大鼠(n = 51)用乌拉坦(1.4 g/kg腹腔注射)麻醉,进行人工通气,并暴露延髓背侧。分离出ADN,在远端切断,将其中心端置于双极刺激电极上。将微量注射到NTS中的10(-7) M ANF的阈剂量与ADN的阈电刺激(n = 37)或微量注射到NTS中的0.13 - 0.5 M Glu的阈剂量(n = 14)相结合。在产生平均动脉压(MAP)和心率[HR;P < 0.05;分别为-20.2 ± 2.3(标准误)mmHg和-30.8 ± 6.9(标准误)次/分钟;n = 18]变化方面,ANF微量注射与ADN刺激之间存在显著相互作用。在产生MAP和HR变化方面,ANF与Glu之间也存在显著相互作用[P < 0.05;分别为-16.3 ± 1.8(标准误)mmHg和-15.0 ± 3.0(标准误)次/分钟;n = 8]。这些结果表明,ANF影响NTS中的神经元,而这些神经元也受动脉压力感受器激活的影响,并且ANF和Glu在NTS中相互作用以产生增强的心血管反应。

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