In Vivo and in Vitro Effects of Angiotensin II on the Release of β-Endorphin-Like Immunoreactivity

• Published in: Endocrinologia Japonica Vol. 32; no. 2; pp. 233 - 240
• Main Authors: MATSUMURA, MITSUHIRO, INOUE, SHUJI, YAMANOI, AKIRA, CHIKAMORI, KAZUMASA, SAITO, SHIRO
• Format: Journal Article
• Language: English
• Published: Tokyo The Japan Endocrine Society 1985; Japan Endocrine Society
• Subjects: Angiotensin II - administration & dosage; Angiotensin II - pharmacology; Animals; beta-Endorphin; Biological and medical sciences; Calcium - pharmacology; Chromatography, Gel; Cobalt - pharmacology; Dose-Response Relationship, Drug; Endorphins - metabolism; Fundamental and applied biological sciences. Psychology; Hormones and neuropeptides. Regulation; Hypothalamus. Hypophysis. Epiphysis. Urophysis; In Vitro Techniques; Injections, Intraventricular; Male; Pituitary Gland, Anterior - drug effects; Pituitary Gland, Anterior - metabolism; Rats; Rats, Inbred Strains; Saralasin - pharmacology; Time Factors; Vertebrates: endocrinology; Calcium; Rat; Secretion; Rodentia; Peptide hormone; Inorganic element; Neuropeptide; Opioid peptide; Biological activity; Vertebrata; Mammalia; Immunoreactive form; Β-Endorphin; Pituitary gland; Angiotensin II
• ISSN: 0013-7219; 2185-6370
• DOI: 10.1507/endocrj1954.32.233

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.