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Titolo:
MECHANISM OF VASOPRESSIN-INDUCED CALCIUM INFLUX IN AORTIC SMOOTH-MUSCLE CELLS - INVOLVEMENT OF CALCIUM-PERMEABLE NONSELECTIVE CATION CHANNEL
Autore:
NAKAJIMA T; HAMADA E; HAZAMA H; WU SN; OMATA M; SEYAMA Y; KURACHI Y;
Indirizzi:
UNIV TOKYO,DEPT INTERNAL MED 2,BUNKYO KU,7-3-1 HONGO TOKYO 113 JAPAN
Titolo Testata:
Heart and vessels
, , anno: 1995, supplemento:, 9
pagine: 65 - 70
SICI:
0910-8327(1995):<65:MOVCII>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Keywords:
VASOPRESSIN; RECEPTOR-OPERATED CALCIUM CHANNEL CA2+; PERMEABLE NONSELECTIVE CATION CHANNEL; AORTIC SMOOTH MUSCLE CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
NO
Recensione:
Indirizzi per estratti:
Citazione:
T. Nakajima et al., "MECHANISM OF VASOPRESSIN-INDUCED CALCIUM INFLUX IN AORTIC SMOOTH-MUSCLE CELLS - INVOLVEMENT OF CALCIUM-PERMEABLE NONSELECTIVE CATION CHANNEL", Heart and vessels, 1995, pp. 65-70

Abstract

The effects of vasopressin on cultured rat aortic smooth muscle cell lines (A7r5) were investigated using the calcium-sensitive dye Indo-1 to measure intracellular calcium ([Ca2+](i)) and the patch-clamp technique in the whole-cell and single-channel configurations. Vasopressin (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 calciumstore release, whereas the latter sustained rise of [Ca2+](i) was dueto calcium entry from outside. The sustained rise of [Ca2+](i) produced by vasopressin, which was not significantly affected by nifedipine 10 mu M, but was completely abolished by La3+ (1 mM). Under the current-clamp condition with K+-containing solution, vasopressin 100 nM produced hyperpolarization followed by depolarization. Under the voltage-clamp condition, at a holding potential of -40mV, vase first activated the outward current followed by a long-lasting inward current with a high noise level. The first outward current elicited by vasopressin wasabolished by charybdotoxin (100 nM) and Cs+ in the patch pipette. In addition, high EGTA (10 mM) in the patch pipette completely abolished the current. Thus, the vasopressin-activated outward current was considered to be the Ca2+-sensitive K+ current (I-K-Ca) The inward current was still elicited with the patch pipette containing Cs+-internal solution, and reversed approximately at 0 mV. The reversal potential was not significantly altered by the replacement of [Cl-](i) or [Cl-](o), suggesting that vasopressin-induced inward current should be non-selective cation channel (I-NS) Extracellularly applied La3+ (1 mM), Cd2+ (1mM) or Mg2+ (10 mM) completely abolished the vasopressin-induced I-NSNifedipine 10 mu M was totally ineffective. I-NS was also observed even when the extracellular cation was Ca2+ or Ba2+. Single-channel activities were recorded in the cell-attached configuration when vasopressin was added to the bathing solution. The unitary conductance of the vasopressin-activated channel was approximately 20 pS with 140 mM Na+, Cs+, or K+ in the patch pipette, but was 15 pS with 110 mM Ca2+ in thepipette. Permeability sequence for sodium calculated from the reversal potential was Na+ is-approximately -equal-to C-s+ is-approximately-equal-to K+ > Ca2+. These results provide evidence that calcium entry elicited by vasopressin is mediated by the receptor-operated Ca2+-permeable non-selective cation channel in aortic smooth muscle cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 05:02:27