Angiotensin ii induced ca2+ mobilization and prolactin release in
normal and hyperplastic pituitary cells.
D[acute]iaz-Torga, Graciela, Arturo Gonz[acute]alez Iglesias, Rita
Ach[acute]aval-Zaia, Carlos Libertun, and Damasia Bec[acute]u
-Villalobos.
Instituto de Biolog[acute]ia y Medicina Experimental. CONICET. V.
Obligado 2490. (1428) Buenos Aires. Telephone: 541-7832869/7843262.
FAX: 541-7862564. EMAIL: dbecu@proteus.dna.uba.ar Established
investigator, CONICET, Argentina. Research fellow, CONICET,
Argentina.
APStracts 4:0250E, 1997.
We evaluated the effects of AII and its antagonists on prolactin
release, intracellular calcium [Ca2+i] mobilization, and
3[H]thymidine uptake in cells from normal rat pituitaries and from
estrogen induced pituitary tumors. AII (10-7 to 10-9 M) increased
prolactin release significantly in control and not in tumoral cells.
In control cells AII (10-6 to 10-9M) produced an immediate spike of
[Ca2+]i followed by a plateau. Spike levels rose significantly
between 10-10 to 10-8M AII, while the onset of the spike was retarded
with decreasing concentrations. In tumoral cells, AII did not produce
a spike phase even at 10-6M. AII-induced prolactin release and
calcium mobilization were blocked by losartan (AT1 antagonist) and
not by PD123319 (AT2 antagonist). Finally, 3[H] thymidine uptake was
not modified by AII (10-7 to 10-10M) or its antagonists in either
group. Our results suggest that chronic in vivo estrogenic treatment
alters in vitro pituitary response to AII. Alterations might function
to limit excessive prolactin secretion of hypersecreting tumors.
Besides, AII does not modify DNA synthesis in vitro of cells from
normal or tumor derived hypophyses.
Received 10 July 1997; accepted in final form 6 November 1997.
APS Manuscript Number E322-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 14 November 1997