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去大脑大鼠对交感神经刺激的血管升压反应特征:嗜铬细胞瘤大鼠中神经刺激和血源性儿茶酚胺刺激的升压反应的差异调节。

Characterization of vasopressor response to sympathetic stimulation in the pithed rat: differential regulation of neuronally stimulated and blood-borne catecholamine-stimulated pressor responses in rats harboring pheochromocytoma.

作者信息

Tsujimoto G, Minegishi A, Ishizaki T, Hoffman B B, Hashimoto K

出版信息

J Pharmacol Exp Ther. 1987 Aug;242(2):637-45.

PMID:2886647
Abstract

The vasopressor response to sympathetic stimulation in the pithed rat was characterized both by analyzing the effects of chemical sympathectomy, adrenalectomy and selective antagonists on the vasopressor response and by measurement of changes in plasma concentrations of catecholamines. Stimulation of the spinal sympathetic outflow evoked a biphasic pressor response: an initial transient component was caused mainly by postganglionic sympathetic nerve stimulation (the direct response); a slowly developing secondary component was mediated predominantly by circulating catecholamines released from the adrenal medulla (the adrenal response). Parallel analysis of plasma catecholamines showed that the rise in epinephrine appeared to be closely related to this adrenal component. The pressor response in adrenalectomized rats was selectively blocked by prazosin but not by yohimbine; however, in sympathectomized rats, the pressor response was abolished by prazosin and yohimbine together but not by either drug given alone. These results suggest that the direct, neurogenic component is mediated mainly by alpha-1 adrenoceptors whereas the secondary, adrenally mediated response occurs by activation of both alpha-1 and alpha-2 adrenoceptors. Furthermore, the in vivo regulation of each component of the pressor response was studied in rats harboring pheochromocytoma (PHEO), a tumor causing marked elevations in endogenous catecholamine concentrations. In PHEO rats, the direct pressor response was found to be relatively intact but the adrenal response was blunted. Inasmuch as there was normal rise in plasma epinephrine to electrical stimulation in PHEO rats, the results suggest a differential regulation of neuronally stimulated and blood-borne catecholamine-mediated pressor responses in PHEO rats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

通过分析化学性交感神经切除术、肾上腺切除术及选择性拮抗剂对升压反应的影响,并测量血浆儿茶酚胺浓度的变化,对脊髓麻醉大鼠对交感神经刺激的升压反应进行了表征。刺激脊髓交感神经传出纤维可诱发双相升压反应:最初的短暂成分主要由节后交感神经刺激引起(直接反应);缓慢发展的次要成分主要由肾上腺髓质释放的循环儿茶酚胺介导(肾上腺反应)。对血浆儿茶酚胺的平行分析表明,肾上腺素的升高似乎与该肾上腺成分密切相关。在肾上腺切除的大鼠中,哌唑嗪可选择性阻断升压反应,而育亨宾则不能;然而,在交感神经切除的大鼠中,哌唑嗪和育亨宾共同作用可消除升压反应,单独使用任何一种药物则无效。这些结果表明,直接的神经源性成分主要由α-1肾上腺素能受体介导,而次要的肾上腺介导反应则通过α-1和α-2肾上腺素能受体的激活而发生。此外,在患有嗜铬细胞瘤(PHEO)的大鼠中研究了升压反应各成分的体内调节,嗜铬细胞瘤是一种导致内源性儿茶酚胺浓度显著升高的肿瘤。在PHEO大鼠中,发现直接升压反应相对完整,但肾上腺反应减弱。由于PHEO大鼠在电刺激下血浆肾上腺素正常升高,结果表明PHEO大鼠中神经刺激和血源性儿茶酚胺介导的升压反应存在差异调节。(摘要截短于250字)

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