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西咪替丁对自发性高血压大鼠的中枢升压活性

Central pressor activity of cimetidine in spontaneously hypertensive rats.

作者信息

Dadkar N K, Aroskar V A, Gupte R D, Dohadwalla A N

出版信息

J Pharm Pharmacol. 1984 Jul;36(7):488-90. doi: 10.1111/j.2042-7158.1984.tb04435.x.

Abstract

The systemic blood pressure effect of cimetidine given intracerebroventricularly (i.c.v.) in anaesthetized spontaneously hypertensive (SH) rats has been investigated. Cimetidine (250 micrograms i.c.v.) caused a gradual long lasting rise in mean arterial blood pressure with maximum of 31.6 +/- 4.5 mm Hg. Chemical degeneration of catecholaminergic neurons with 6-OHDA treatment, central administration of phentolamine and prazosin, and the bilateral adrenalectomy significantly inhibited the pressor response of cimetidine, while propranolol (i.c.v.) had no effect. From these results it appears that the hypertensive response of cimetidine is mediated by central catecholaminergic pathways and is due to an increase in efferent sympathetic outflow and release of catecholamine from the adrenal medulla.

摘要

研究了在麻醉的自发性高血压(SH)大鼠中脑室内(i.c.v.)给予西咪替丁对全身血压的影响。西咪替丁(脑室内注射250微克)导致平均动脉血压逐渐持久升高,最高可达31.6±4.5毫米汞柱。用6-OHDA处理使儿茶酚胺能神经元发生化学性退变、中枢给予酚妥拉明和哌唑嗪以及双侧肾上腺切除术均显著抑制了西咪替丁的升压反应,而普萘洛尔(脑室内注射)则无作用。从这些结果看来,西咪替丁的高血压反应是由中枢儿茶酚胺能途径介导的,并且是由于传出交感神经传出增加以及肾上腺髓质儿茶酚胺释放所致。

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