Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells

In rat pituitary cells from estrogen-induced hyperplasia, angiotensin II (ANG II) does not evoke a clear spike elevation of intracellular Ca2+ concentration ([Ca2+](i)) but induces a plateau increase. The present work was undertaken to establish whether this difference was related to a differential...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Iglesias, A.G., Diaz-Torga, G., Lux-Lantos, V., Libertun, C., Becu-Villalobos, D.
Formato: JOUR
Materias:
rat
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_01931849_v277_n340-3_pE455_Iglesias
Aporte de:
id todo:paper_01931849_v277_n340-3_pE455_Iglesias
record_format dspace
spelling todo:paper_01931849_v277_n340-3_pE455_Iglesias2023-10-03T15:09:13Z Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells Iglesias, A.G. Diaz-Torga, G. Lux-Lantos, V. Libertun, C. Becu-Villalobos, D. Estrogen Inositol trisphosphate Nifedipine Thapsigargin angiotensin calcium channel calcium ion estrogen inositol trisphosphate nifedipine thapsigargin animal cell article calcium cell level calcium homeostasis calcium mobilization calcium transport cell hyperplasia controlled study estrus cycle female hypophysis cell nonhuman phosphoinositide metabolism priority journal rat Angiotensin II Animals Calcium Calcium Channel Blockers Calcium Channels, L-Type Female Hyperplasia Inositol 1,4,5-Trisphosphate Intracellular Membranes Pituitary Gland Potassium Rats Rats, Sprague-Dawley Reference Values Thapsigargin In rat pituitary cells from estrogen-induced hyperplasia, angiotensin II (ANG II) does not evoke a clear spike elevation of intracellular Ca2+ concentration ([Ca2+](i)) but induces a plateau increase. The present work was undertaken to establish whether this difference was related to a differential participation of intracellular and/or plasma membrane Ca2+ channels. We first tested the effect of 10 nM ANG II on [Ca2+](i) in the absence of extracellular Ca2+ in cells depolarized with 25 mM K+ or in the presence of blockers of L-type voltage-sensitive Ca2+ channels (VSCC). These treatments did not alter spike elevation in [Ca2+](i) in controls but reduced plateau levels in hyperplastic cells. Intracellular Ca2+ stores were similar in both groups, as assessed by thapsigargin treatment, but this drug abolished spike increase in controls and scarcely modified plateau levels in hyperplastic cells. Finally, inositol trisphosphate (InsP3) production in response to ANG II was significantly higher in control cells. We conclude that the observed plateau rise in hyperplastic cells results mainly from Ca2+ influx through VSCC. In contrast, in control cells, the ANG II-induced spike increase in [Ca2+](i) results from mobilization of Ca2+ from thapsigargin-sensitive internal channels, activated by higher inositol 1,4,5-trisphosphate generation. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_01931849_v277_n340-3_pE455_Iglesias
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Estrogen
Inositol trisphosphate
Nifedipine
Thapsigargin
angiotensin
calcium channel
calcium ion
estrogen
inositol trisphosphate
nifedipine
thapsigargin
animal cell
article
calcium cell level
calcium homeostasis
calcium mobilization
calcium transport
cell hyperplasia
controlled study
estrus cycle
female
hypophysis cell
nonhuman
phosphoinositide metabolism
priority journal
rat
Angiotensin II
Animals
Calcium
Calcium Channel Blockers
Calcium Channels, L-Type
Female
Hyperplasia
Inositol 1,4,5-Trisphosphate
Intracellular Membranes
Pituitary Gland
Potassium
Rats
Rats, Sprague-Dawley
Reference Values
Thapsigargin
spellingShingle Estrogen
Inositol trisphosphate
Nifedipine
Thapsigargin
angiotensin
calcium channel
calcium ion
estrogen
inositol trisphosphate
nifedipine
thapsigargin
animal cell
article
calcium cell level
calcium homeostasis
calcium mobilization
calcium transport
cell hyperplasia
controlled study
estrus cycle
female
hypophysis cell
nonhuman
phosphoinositide metabolism
priority journal
rat
Angiotensin II
Animals
Calcium
Calcium Channel Blockers
Calcium Channels, L-Type
Female
Hyperplasia
Inositol 1,4,5-Trisphosphate
Intracellular Membranes
Pituitary Gland
Potassium
Rats
Rats, Sprague-Dawley
Reference Values
Thapsigargin
Iglesias, A.G.
Diaz-Torga, G.
Lux-Lantos, V.
Libertun, C.
Becu-Villalobos, D.
Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
topic_facet Estrogen
Inositol trisphosphate
Nifedipine
Thapsigargin
angiotensin
calcium channel
calcium ion
estrogen
inositol trisphosphate
nifedipine
thapsigargin
animal cell
article
calcium cell level
calcium homeostasis
calcium mobilization
calcium transport
cell hyperplasia
controlled study
estrus cycle
female
hypophysis cell
nonhuman
phosphoinositide metabolism
priority journal
rat
Angiotensin II
Animals
Calcium
Calcium Channel Blockers
Calcium Channels, L-Type
Female
Hyperplasia
Inositol 1,4,5-Trisphosphate
Intracellular Membranes
Pituitary Gland
Potassium
Rats
Rats, Sprague-Dawley
Reference Values
Thapsigargin
description In rat pituitary cells from estrogen-induced hyperplasia, angiotensin II (ANG II) does not evoke a clear spike elevation of intracellular Ca2+ concentration ([Ca2+](i)) but induces a plateau increase. The present work was undertaken to establish whether this difference was related to a differential participation of intracellular and/or plasma membrane Ca2+ channels. We first tested the effect of 10 nM ANG II on [Ca2+](i) in the absence of extracellular Ca2+ in cells depolarized with 25 mM K+ or in the presence of blockers of L-type voltage-sensitive Ca2+ channels (VSCC). These treatments did not alter spike elevation in [Ca2+](i) in controls but reduced plateau levels in hyperplastic cells. Intracellular Ca2+ stores were similar in both groups, as assessed by thapsigargin treatment, but this drug abolished spike increase in controls and scarcely modified plateau levels in hyperplastic cells. Finally, inositol trisphosphate (InsP3) production in response to ANG II was significantly higher in control cells. We conclude that the observed plateau rise in hyperplastic cells results mainly from Ca2+ influx through VSCC. In contrast, in control cells, the ANG II-induced spike increase in [Ca2+](i) results from mobilization of Ca2+ from thapsigargin-sensitive internal channels, activated by higher inositol 1,4,5-trisphosphate generation.
format JOUR
author Iglesias, A.G.
Diaz-Torga, G.
Lux-Lantos, V.
Libertun, C.
Becu-Villalobos, D.
author_facet Iglesias, A.G.
Diaz-Torga, G.
Lux-Lantos, V.
Libertun, C.
Becu-Villalobos, D.
author_sort Iglesias, A.G.
title Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
title_short Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
title_full Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
title_fullStr Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
title_full_unstemmed Calcium influx and intracellular stores in angiotensin II stimulation of normal and hyperplastic pituitary cells
title_sort calcium influx and intracellular stores in angiotensin ii stimulation of normal and hyperplastic pituitary cells
url http://hdl.handle.net/20.500.12110/paper_01931849_v277_n340-3_pE455_Iglesias
work_keys_str_mv AT iglesiasag calciuminfluxandintracellularstoresinangiotensiniistimulationofnormalandhyperplasticpituitarycells
AT diaztorgag calciuminfluxandintracellularstoresinangiotensiniistimulationofnormalandhyperplasticpituitarycells
AT luxlantosv calciuminfluxandintracellularstoresinangiotensiniistimulationofnormalandhyperplasticpituitarycells
AT libertunc calciuminfluxandintracellularstoresinangiotensiniistimulationofnormalandhyperplasticpituitarycells
AT becuvillalobosd calciuminfluxandintracellularstoresinangiotensiniistimulationofnormalandhyperplasticpituitarycells
_version_ 1807317702041141248