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

We evaluated the effects of angiotensin II (ANG II) and its antagonists on prolactin release, intracellular calcium ([Ca2+](i)) mobilization, and [3H]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...

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Publicado: 1998
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01931849_v274_n337-3_pE534_DiazTorga
http://hdl.handle.net/20.500.12110/paper_01931849_v274_n337-3_pE534_DiazTorga
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spelling paper:paper_01931849_v274_n337-3_pE534_DiazTorga2023-06-08T15:20:02Z Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells Calcium Estrogen angiotensin angiogenesis animal cell article calcium mobilization cell hyperplasia DNA synthesis inhibition drug receptor binding enzyme activation hormone release hypophysis cell immediate early gene nonhuman priority journal prolactin release promoter region rat renin angiotensin aldosterone system tumor growth We evaluated the effects of angiotensin II (ANG II) and its antagonists on prolactin release, intracellular calcium ([Ca2+](i)) mobilization, and [3H]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 [Ca2+](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 (AT1 receptor antagonist) and not by PD-123319 (AT2 antagonist). Finally, [3H]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. 1998 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01931849_v274_n337-3_pE534_DiazTorga http://hdl.handle.net/20.500.12110/paper_01931849_v274_n337-3_pE534_DiazTorga
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Calcium
Estrogen
angiotensin
angiogenesis
animal cell
article
calcium mobilization
cell hyperplasia
DNA synthesis inhibition
drug receptor binding
enzyme activation
hormone release
hypophysis cell
immediate early gene
nonhuman
priority journal
prolactin release
promoter region
rat
renin angiotensin aldosterone system
tumor growth
spellingShingle Calcium
Estrogen
angiotensin
angiogenesis
animal cell
article
calcium mobilization
cell hyperplasia
DNA synthesis inhibition
drug receptor binding
enzyme activation
hormone release
hypophysis cell
immediate early gene
nonhuman
priority journal
prolactin release
promoter region
rat
renin angiotensin aldosterone system
tumor growth
Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
topic_facet Calcium
Estrogen
angiotensin
angiogenesis
animal cell
article
calcium mobilization
cell hyperplasia
DNA synthesis inhibition
drug receptor binding
enzyme activation
hormone release
hypophysis cell
immediate early gene
nonhuman
priority journal
prolactin release
promoter region
rat
renin angiotensin aldosterone system
tumor growth
description We evaluated the effects of angiotensin II (ANG II) and its antagonists on prolactin release, intracellular calcium ([Ca2+](i)) mobilization, and [3H]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 [Ca2+](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 (AT1 receptor antagonist) and not by PD-123319 (AT2 antagonist). Finally, [3H]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.
title Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
title_short Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
title_full Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
title_fullStr Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
title_full_unstemmed Angiotensin II-induced Ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
title_sort angiotensin ii-induced ca2+ mobilization and prolactin release in normal and hyperplastic pituitary cells
publishDate 1998
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01931849_v274_n337-3_pE534_DiazTorga
http://hdl.handle.net/20.500.12110/paper_01931849_v274_n337-3_pE534_DiazTorga
_version_ 1768542265481887744