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Titolo:
ENDOTHELIN-1 AND VASOPRESSIN ACTIVATE CA2-PERMEABLE NONSELECTIVE CATION CHANNELS IN AORTIC SMOOTH-MUSCLE CELLS - MECHANISM OF RECEPTOR-MEDIATED CA2+ INFLUX()
Autore:
NAKAJIMA T; HAZAMA H; HAMADA E; WU SN; IGARASHI K; YAMASHITA T; SEYAMA Y; OMATA M; KURACHI Y;
Indirizzi:
UNIV TOKYO,DEPT INTERNAL MED 2,FAC MED,BUNKYO KU,7-3-1 HONGO TOKYO 113 JAPAN UNIV TOKYO,DEPT PHYSIOL CHEM & NUTR,BUNKYO KU TOKYO 113 JAPAN OSAKA UNIV,DEPT PHARMACOL 2 SUITA OSAKA 565 JAPAN
Titolo Testata:
Journal of Molecular and Cellular Cardiology
fascicolo: 4, volume: 28, anno: 1996,
pagine: 707 - 722
SICI:
0022-2828(1996)28:4<707:EAVACN>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG ILEUM; RABBIT PORTAL-VEIN; INOSITOL TRISPHOSPHATE; PHOSPHOLIPASE-C; DEPENDENT CA-2+; PRIMARY CULTURE; K+ CHANNEL; G-PROTEIN; CALCIUM; RAT;
Keywords:
VASCULAR SMOOTH MUSCLE CELLS; A CA2+ -PERMEABLE NONSELECTIVE CATION CHANNEL; VASOPRESSIN; ENDOTHELIN-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
T. Nakajima et al., "ENDOTHELIN-1 AND VASOPRESSIN ACTIVATE CA2-PERMEABLE NONSELECTIVE CATION CHANNELS IN AORTIC SMOOTH-MUSCLE CELLS - MECHANISM OF RECEPTOR-MEDIATED CA2+ INFLUX()", Journal of Molecular and Cellular Cardiology, 28(4), 1996, pp. 707-722

Abstract

The effects of vasopressin and endothelin-1 on cultured aortic smoothmuscle cell lines (A7r5) were investigated by measurements of intracellular calcium [Ca2+](i) and the patch-damp techniques. Vasopressin and endothelin-1 (100 nM) evoked an initial peak followed by a smaller sustained rise of [Ca2+](i) in the presence of extracellular calcium [Ca2+](o). In the absence of [Ca2+](o), only the initial peak of [Ca2+](i) was observed. Therefore, the initial peak of [Ca2+](i) was mainly due to calcium release from the storage sites, whereas the later sustained rise of [Ca2+](i) was due to the calcium entry from outside. The sustained rise of [Ca2+](i) was unaffected by nifedipine (10 mu M) significantly, but was completely abolished by La3+ (1 mM). Under current clamp conditions with K+-internal solution, vasopressin and endothelin-1 (100 nM) produced hyperpolarization, then followed by depolarization. Under voltage clamp conditions at a holding potential of -40 mV, both vasopressin and endothelin-1 first activated the outward current, then followed by a long-lasting inward current with a high noise level. The first outward current was abolished by charybdotoxin (100 nM), Cs in the patch pipette and high EGTA (10 mM) in the pipette, suggesting that it was a Ca2+-sensitive K+ current (i(K.Ca)). The inward current was still elicited with the patch pipette containing Cs+-internal solution, and reversed at about 0 mV. The reversal potential was not significantly altered by the replacement of [Cl-](i) or [Cl-](o), proposing that the inward current is a cation selective channel (I-N.S.). Theinward current was also observed even when extracellular cations are Ca2+. La3+ (1 mM), Cd2+ (1 mM) completely abolished the vasopressin-induced I-N.S., however, nifedipine (10 mu M) failed to inhibit it significantly. Single channel activities were recorded in the cell-attachedconfigurations when vasopressin or endothelin-l was applied to the bathing solution. The unitary conductance of the channels was approximately 20 pS with 140 mM Na+, Cs+, or K+ in the pipette, but was 15 pS with 110 mM Ca2+ in the pipette. Permeabilities sequence calculated fromthe reversal potentials was Na+ Cs+ K+ Ca+. These results provide evidence that calcium entry and membrane depolarization elicited by vasopressin or endothelin-1 are mediated by a receptormediated Ca2+-permeable non-selectire cation channel in aortic smooth muscle cells. (C) 1990 Academie Press Limited

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Documento generato il 06/04/20 alle ore 05:41:08