Effect of Angiotensin II on in Vivo and in Vitro Release of Anterior Pituitary Hormones in the Female Rat*

Ovariectomized female rats bearing implanted third ventricular cannulae were injected with 2 μl 0.9% NaCl or 2 μl saline containing 5 μg Angiotensin II (AII) or 25 μg saralasin, an AII antagonist. Plasma PRL, GH, LH, and TSH levels were measured by RIA in jugular blood samples drawn through indwelling silastic cannulae while the animals were conscious and freely moving in their cages. Third ventricular injections of AII depressed both PRL and GH levels within 15 min of drug administration, with levels remaining suppressed for up to 1 h. Pretreatment of animals with saralasin slightly elevated basal PRL levels and completely blocked both the PRL- and GH-lowering effects of AII Concentrations of LH and TSH in plasma were not altered by intraventricular AII compared to those of saline-injected control animals. Saralasin alone, on the other hand, decreased plasma TSH levels. Intravenous injection of AII (5 μg/100 μ saline) produced a rise within 5 min in PRL levels, followed by a progressive decline thereafter. Levels of GH were reduced only at 30 min, while values of TSH and LH were unchanged relative to preinjection concentrations. Injection of 100 μl of saline iv had no effects upon plasma hormone levels. In vitro incubation of hemipituitaries with doses of AII ranging from 0.5–50.0 μg/flask increased LH, GH, and PRL levels at different doses after 180 min. LH was stimulated with the 0.5-and 5-μg doses of AII. GH release was enhanced by the 5-μg dose and PRL by the highest dose tested (50 μg). TSH concentrations were significantly elevated by the two largest doses (5.0 and 50.0 μg AII/flask) at 30, 60, 120, and 180 min of incubation. These data suggest that AII may be involved in the regulation of PRL, GH, and TSH secretion. The effects on TSH may be due to a direct action upon the pituitary, whereas the depressant effects of AII on PRL and GH release are probably mediated by hypothalamic mechanisms. Additional studies should determine whether AII is physiologically involved in the regulation of the secretion of these hormones.