Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells

Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas V, Obligado 2490, (1428) Buenos Aires, Argentina We evaluated the effects of angiotensin II (ANG II) and its antagonists on prolactin release, intracellular calcium ([Ca 2+ ] i ) mobilization, a...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of physiology: endocrinology and metabolism Vol. 274; no. 3; p. E534
Main Authors Diaz-Torga, Graciela, Iglesias, Arturo Gonzalez, Achaval-Zaia, Rita, Libertun, Carlos, Becu-Villalobos, Damasia
Format Journal Article
LanguageEnglish
Published United States 01.03.1998
Subjects
Angiotensin II - pharmacology
Animals
Calcium - metabolism
Cells, Cultured
DNA Replication
Estrogens
Female
Hyperplasia - metabolism
Pituitary Gland, Anterior - drug effects
Pituitary Gland, Anterior - metabolism
Pituitary Neoplasms - metabolism
Prolactin - metabolism
Prolactinoma - metabolism
Rats
Rats, Sprague-Dawley
Thymidine - pharmacokinetics
Online AccessGet full text

Cover

More Information
Summary:Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas V, Obligado 2490, (1428) Buenos Aires, Argentina We evaluated the effects of angiotensin II (ANG II) and its antagonists on prolactin release, intracellular calcium ([Ca 2+ ] i ) mobilization, and [ 3 H]thymidine uptake in cells from normal rat pituitaries and from estrogen-induced pituitary tumors. ANG II (10 7 to 10 9 M) increased prolactin release significantly in control and not in tumoral cells. In control cells, ANG II (10 6 to 10 9 M) produced an immediate spike of [Ca 2+ ] i followed by a plateau. Spike levels rose significantly between 10 10 and 10 8 M ANG II, whereas the onset of the spike was retarded with decreasing concentrations. In tumoral cells, ANG II did not produce a spike phase even at 10 6 M. ANG II-induced prolactin release and calcium mobilization were blocked by losartan (AT 1 receptor antagonist) and not by PD-123319 (AT 2 antagonist). Finally, [ 3 H]thymidine uptake was not modified by ANG II (10 7 to 10 10 M) or its antagonists in either group. Our results suggest that chronic in vivo estrogenic treatment alters in vitro pituitary response to ANG II. Alterations might function to limit excessive prolactin secretion of hypersecreting tumors. Besides, ANG II does not modify DNA synthesis in vitro of cells from normal or tumor-derived hypophyses. calcium; estrogen
ISSN:0193-1849
0002-9513
1522-1555
DOI:10.1152/ajpendo.1998.274.3.E534