Abstract
The effect of angiotensin II (A II) on the release of β-endorphin-like immunoreactivity (β-END-LI) in rats was studied in vivo and in vitro. Intravenous injection of 1μg/100g body weight of A II resulted in significant increase in the plasma β-END-LI level after 10 and 20min. Intraventricular injection of 1ng/100g body weight of A II also resulted in significant increase in the plasma β-END-LI level after 10min. A II at concentrations of 10-12M-10-10M caused dose-dependent stimulation of β-END-LI release from dispersed cells of rat anterior pituitary. On gel chromatography, the β-END-LI released by incubation of the cells with 10-10M A II separated into two components which eluted in the same positions as human β-lipotropin and human β-endorphin, respectively. The ratio of β-LPH to β-END in these fractions was 5: 1 on a molar basis. A II did not stimulate β-END-LI release in Ca++-free-medium.[Sar1 Ala8]-A II at concentrations of 10-9M-10-7M did not stimulate β-ENDLI release from the cells. Addition of [Sar1, Ala8]-A II to the incubation medium inhibited A II-induced β-END-LI release from the cells.
These results indicate that A II acts, at least in part, directly on anterior pituitary cells to stimulate β-END-LI release and that calcium ion is involved in the mechanism of this effect.
