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Titolo:
DOES TYROSINE KINASE MODULATE DELAYED-RECTIFIER K-CHANNELS IN GUINEA-PIG VENTRICULAR CELLS
Autore:
WASHIZUKA T; HORIE M; OBAYASHI K; SASAYAMA S;
Indirizzi:
KYOTO UNIV,GRAD SCH MED,DEPT CARDIOVASC MED,SAKYO KU,54 SHOGOIN KAWARAMACHI KYOTO 60601 JAPAN KYOTO UNIV,GRAD SCH MED,DEPT CARDIOVASC MED,SAKYO KU KYOTO 60601 JAPAN
Titolo Testata:
Heart and vessels
, , anno: 1997, supplemento:, 12
pagine: 173 - 174
SICI:
0910-8327(1997):<173:DTKMDK>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC MYOCYTES; CURRENTS;
Keywords:
GENISTEIN; TYROSINE KINASE; DELAYED RECTIFIER POTASSIUM CURRENT;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
10
Recensione:
Indirizzi per estratti:
Citazione:
T. Washizuka et al., "DOES TYROSINE KINASE MODULATE DELAYED-RECTIFIER K-CHANNELS IN GUINEA-PIG VENTRICULAR CELLS", Heart and vessels, 1997, pp. 173-174

Abstract

Phosphorylation by tyrosine kinases has been shown to promote cellular growth and hypertrophy and to play a key role in modulating ion channels. We have examined possible effects of genistein, a protein tyrosine kinase (PTK) inhibitor, on cardiac delayed-rectifier K currents (I-K). Guinea pig ventricular were voltage-clamped by conventional mode (5.4 mM [K](out)/150 mM [K](in); pCa = 8; 36 degrees C). Amplitudes of tail and steady-state (2-s pulse) currents were measured as I,. Micromolar concentrations of genistein (10-100 mu M) reversibly inhibited basal, swelling-enhanced (by 70% hypotonic solution), and intrapipette Cyclic adenosine monophosphate (cAMP) (1 mM)-enhanced I-K concentration-dependently, while intrapipette cAMP-enhanced I-K were also affected by daidzein, an inactive analog of genistein. In contrast, lavendustinA (10 mu M) and tyrphostin 51. (100 mu M), other types of PTK inhibitors, had no effect on I-K. These results suggest that genistein may inhibit I-K and that this inhibition is not mediated by an inhibition oftyrosine kinase activity.

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Documento generato il 11/08/20 alle ore 15:33:39