Publication Date:
1991-09-13
Description:
The phosphorylation of the cardiac sodium channel by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase A leads to its inactivation. It was shown that extracellular cAMP can also modulate the sodium channel of rat, guinea pig, and frog ventricular myocytes in a rapid (less than 50 milliseconds), reversible, and dose-dependent manner. The decrease in the sodium current was accompanied by a 10- to 15-millivolt shift in the steady-state availability of the sodium channel toward more negative potentials and was inhibited by guanosine-5'-O-(2-thiodiphosphate) or pertussis toxin, suggesting that the extracellular modulation of the sodium channel by cAMP is mediated by a membrane-delimited mechanism that includes a pertussis toxin-sensitive G protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorbera, L A -- Morad, M -- HL16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 13;253(5025):1286-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1653970" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Cyclic AMP/*pharmacology
;
Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
;
Guanosine Diphosphate/analogs & derivatives/pharmacology
;
Guinea Pigs
;
Heart/drug effects/*physiology
;
Isoproterenol/pharmacology
;
Kinetics
;
Membrane Potentials/drug effects
;
Pertussis Toxin
;
Rana pipiens
;
Rats
;
Receptors, Cyclic AMP/drug effects/*physiology
;
Sodium Channels/drug effects/*physiology
;
Thionucleotides/pharmacology
;
Virulence Factors, Bordetella/pharmacology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
