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室旁核损伤对饮水及对血管紧张素II升压反应的影响。

Effect of paraventricular nucleus lesions on drinking and pressor responses to ANG II.

作者信息

Gutman M B, Jones D L, Ciriello J

机构信息

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

出版信息

Am J Physiol. 1988 Dec;255(6 Pt 2):R882-7. doi: 10.1152/ajpregu.1988.255.6.R882.

Abstract

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

摘要

进行实验以研究下丘脑室旁核(PVH)的细胞对清醒无束缚大鼠脑穹窿下器(SFO)微量注射血管紧张素II(ANG II)所引发的饮水和升压反应的作用。微量注射ANG II(5微克溶于0.2微升)引发饮水反应(15分钟内7.1±0.7毫升,n = 18)和升压反应(19±1毫米汞柱,n = 17)。通过注射 kainic 酸(KA;0.2微克溶于0.2微升磷酸盐缓冲液)对PVH进行双侧损伤,导致饮水反应消失(损伤前15分钟内7.8±1.8毫升;损伤后15分钟内0毫升,n = 6),并且升压反应显著(P<0.05)减弱(损伤前15±1毫米汞柱;损伤后5±2毫米汞柱,n = 5)。双侧向PVH注射0.2微升磷酸盐缓冲液载体以及向PVH相邻区域注射KA对饮水或升压反应无显著影响。与向相邻非PVH组织注射KA的动物(n = 7)或向PVH注射载体的动物(n = 5)相比,向PVH注射KA导致PVH后背部小细胞丢失70 - 80%。这些结果表明,PVH的小细胞是介导对作用于SFO的ANG II产生饮水和升压反应的神经回路的重要组成部分。

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