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血管紧张素II诱导的加压素释放受到中枢心房利钠因子的抑制。

Angiotensin II-induced vasopressin release is attenuated by central atrial natriuretic factor.

作者信息

Casto R, Keiler I, Schroeder G, Stock G

出版信息

Clin Exp Hypertens A. 1987;9(1):81-94. doi: 10.3109/10641968709160031.

Abstract

Administration of angiotensin II (Ang II) into the cerebral ventricles (icv) of rats elicits vasopressin release and an increase in blood pressure. The effect of atrial natriuretic factor (ANF) on these actions of ANG II was studied in conscious spontaneously hypertensive rats. The magnitude and time course of the blood pressure increase following ANG II (50 and 100 ng) were not altered by ANF, icv. However, vasopressin levels which were stimulated from 10.8 +/- 1.5 to 62.1 +/- 6.4 pq/ml by ANG II (100 ng) were significantly suppressed by combined administration of ANG II (100 ng) and ANF (3 ug/kg) (33.0 +/- 4.3 pg/ml). The injection of ANF alone into the cerebral ventricles had no effect on resting blood pressure or vasopressin levels. Peripheral administration of ANF was unable to attenuate the ANG II-induced vasopressin release. These data suggest that there exists a central interaction of ANF and ANG II within the brain which cannot be mimicked by peripheral administration of ANF.

摘要

向大鼠脑室内注射血管紧张素II(Ang II)会引发血管加压素释放并导致血压升高。在清醒的自发性高血压大鼠中研究了心房利钠因子(ANF)对Ang II这些作用的影响。脑室内注射ANF不会改变Ang II(50和100 ng)引起的血压升高幅度和时间进程。然而,Ang II(100 ng)可使血管加压素水平从10.8±1.5升高至62.1±6.4 pg/ml,联合注射Ang II(100 ng)和ANF(3 μg/kg)可显著抑制血管加压素水平(33.0±4.3 pg/ml)。单独向脑室内注射ANF对静息血压或血管加压素水平无影响。外周注射ANF无法减弱Ang II诱导的血管加压素释放。这些数据表明,脑内存在ANF与Ang II的中枢相互作用,外周注射ANF无法模拟这种相互作用。

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