心房利钠多肽可减弱中枢性血管紧张素II诱导的儿茶酚胺和促肾上腺皮质激素分泌。

Atrial natriuretic polypeptide attenuates central angiotensin II-induced catecholamine and ACTH secretion.

作者信息

Makino S, Hashimoto K, Ota Z

机构信息

3rd Department of Internal Medicine, Okayama University Medical School, Japan.

出版信息

Brain Res. 1989 Oct 30;501(1):84-9. doi: 10.1016/0006-8993(89)91029-9.

DOI:10.1016/0006-8993(89)91029-9

PMID:2553215

Abstract

The interaction between angiotensin II (AII) and synthetic atrial natriuretic polypeptide (ANP) on the sympathetic nervous system and ACTH secretion was examined in unanesthetized, freely moving rats. Centrally administered AII (100 ng/2 microliters) caused hypertension with elevation of the plasma epinephrine level. Central administration of ANP (3 micrograms/3 microliters, 10 micrograms/3 microliters) attenuated central AII-induced pressor response and plasma epinephrine elevation. Furthermore, central AII stimulated ACTH secretion, and ANP reduced the ACTH secretion induced by AII. These results show that ANP attenuates the central AII-induced pressor response at least partially by suppressing sympathetic nervous activity, and ANP regulates ACTH secretion at the hypothalamic level.

摘要

在未麻醉、自由活动的大鼠中，研究了血管紧张素II（AII）与合成心房利钠多肽（ANP）对交感神经系统和促肾上腺皮质激素（ACTH）分泌的相互作用。中枢给予AII（100 ng/2微升）导致高血压，并伴有血浆肾上腺素水平升高。中枢给予ANP（3微克/3微升、10微克/3微升）可减弱中枢AII诱导的升压反应和血浆肾上腺素升高。此外，中枢给予AII刺激ACTH分泌，而ANP可降低AII诱导的ACTH分泌。这些结果表明，ANP至少部分通过抑制交感神经活动来减弱中枢AII诱导的升压反应，并且ANP在下丘脑水平调节ACTH分泌。