Document Detail


Genistein increases the sensitivity of cardiac ion channels to beta-adrenergic receptor stimulation.
MedLine Citation:
PMID:  9670916     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The whole-cell patch-clamp technique was used to monitor the effects of genistein, a tyrosine kinase inhibitor, on membrane currents recorded from isolated guinea pig ventricular myocytes. Under control conditions, genistein (50 micromol/L) did not activate the latent cAMP-regulated Cl- current (ICl). However, in the presence of a subthreshold concentration (1 nmol/L) of the beta-adrenergic agonist isoproterenol (Iso), genistein caused a near-maximal activation of this current. In the absence of genistein, Iso activated ICl with an EC50 of 5 nmol/L. In the presence of genistein, Iso activated ICl with an EC50 of 0.3 nmol/L. This facilitatory effect was not observed in the presence of daidzein (50 micromol/L), an analogue of genistein that only weakly inhibits tyrosine kinase activity. Furthermore, peroxovanadate, a potent inhibitor of phosphotyrosine phosphatase activity, inhibited ICl activated by Iso alone, and it blocked the stimulatory effect of genistein in the presence of Iso. To determine whether the stimulatory effect of genistein was specific for ICl, we also studied its action on the cAMP-regulated delayed rectifier K+ current (IK) and L-type Ca2+ current (ICa-L) present in these cells. Basal IK and ICa-L were partially (approximately 30% to 40%) inhibited by genistein. However, this inhibitory effect was mimicked by daidzein, suggesting that inhibition of tyrosine kinase activity is not involved. In addition to the nonspecific inhibitory effect, genistein also caused a significant increase in the beta-adrenergic sensitivity of the unblocked cationic currents. In the absence of genistein, 1 nmol/L Iso had no effect on either IK or ICa-L. However, in the presence of genistein, 1 nmol/L Iso significantly increased the magnitude of both currents. These results suggest that tyrosine kinase activity may play an important role in regulating beta-adrenergic responsiveness of the heart.
Authors:
L C Hool; L M Middleton; R D Harvey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation research     Volume:  83     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-08-13     Completed Date:  1998-08-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  33-42     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology*
Animals
Calcium / physiology
Chlorides / physiology
Cyclic AMP / physiology
Cystic Fibrosis Transmembrane Conductance Regulator / physiology
Electric Conductivity
Enzyme Inhibitors / pharmacology*
Genistein / pharmacology*
Guinea Pigs
Ion Channels / drug effects*
Isoproterenol / pharmacology*
Myocardium / metabolism*
Patch-Clamp Techniques
Potassium / physiology
Protein-Tyrosine Kinases / antagonists & inhibitors,  physiology
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Chlorides; 0/Enzyme Inhibitors; 0/Ion Channels; 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator; 446-72-0/Genistein; 60-92-4/Cyclic AMP; 7440-09-7/Potassium; 7440-70-2/Calcium; 7683-59-2/Isoproterenol; EC 2.7.10.1/Protein-Tyrosine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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