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Titolo:
Nifedipine-activated Ca2+ permeability in newborn rat cortical collecting duct cells in primary culture
Autore:
Valencia, L; Bidet, M; Martial, S; Sanchez, E; Melendez, E; Tauc, M; Poujeol, C; Martin, D; Namorado, MD; Reyes, JL; Poujeol, P;
Indirizzi:
Univ Nice Sophia Antipolis, CNRS, UMR6548, F-06108 Nice 2, France Univ Nice Sophia Antipolis Nice France 2 UMR6548, F-06108 Nice 2, France Inst Politecn Nacl, Ctr Invest & Estudios Avanzados, Dept Fisiol, Mexico City 07000, DF, Mexico Inst Politecn Nacl Mexico City DF Mexico 07000 ico City 07000, DF, Mexico
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 5, volume: 280, anno: 2001,
pagine: C1193 - C1203
SICI:
0363-6143(200105)280:5<C1193:NCPINR>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR MESSENGER-RNA; CALCIUM-CHANNEL; CONVOLUTED TUBULE; METABOLIC INHIBITION; VENTRICULAR MYOCYTES; PARATHYROID-HORMONE; CYTOSOLIC CALCIUM; NEPHRON SEGMENTS; RENAL TUBULES; LEAK CHANNEL;
Keywords:
calcium channel; dihydropyridine; kidney; newborn;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Poujeol, P Univ Nice Sophia Antipolis, CNRS, UMR6548, Parc Valrose, F-06108 Nice 2, France Univ Nice Sophia Antipolis Parc Valrose Nice France 2 , France
Citazione:
L. Valencia et al., "Nifedipine-activated Ca2+ permeability in newborn rat cortical collecting duct cells in primary culture", AM J P-CELL, 280(5), 2001, pp. C1193-C1203

Abstract

To characterize Ca2+ transport in newborn rat cortical collecting duct (CCD) cells, we used nifedipine, which in adult rat distal tubules inhibits the intracellular Ca2+ concentration ([Ca2+](i)) increase in response to hormonal activation. We found that the dihydropyridine (DHP) nifedipine (20 muM) produced an increase in [Ca2+](i) from 87.6 +/- 3.3 nM to 389.9 +/- 29.0 nM in 65% of the cells. Similar effects of other DHP (BAY K 8644, isradipine) were also observed. Conversely, DHPs did not induce any increase in [Ca2](i) in cells obtained from proximal convoluted tubule. In CCD cells, neither verapamil nor diltiazem induced any rise in [Ca2+](i). Experiments in the presence of EGTA showed that external Ca2+ was required for the nifedipine effect, while lanthanum (20 mM), gadolinium (100 mM), and diltiazem (20 mM) inhibited the effect. Experiments done in the presence of valinomycin resulted in the same nifedipine effect, showing that K+ channels were not involved in the nifedipine-induced [Ca2+](i) rise. H2O2 also triggered [Ca2+](i) rise. However, nifedipine-induced [Ca2+](i) increase was not affected by protamine. In conclusion, the present results indicate that 1) primary cultures of cells from terminal nephron of newborn rats are a useful tool forinvestigating Ca2+ transport mechanisms during growth, and 2) newborn rat CCD cells in primary culture exhibit a new apical nifedipine-activated Ca2channel of capacitive type (either transient receptor potential or leak channel).

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Documento generato il 22/01/20 alle ore 18:30:04