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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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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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 |
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1768542265481887744 |