Halothane interaction with guanine nucleotide binding proteins in mouse heart.
Volatile anesthetics have been shown to decrease hormone-induced adenosine cyclic monophosphate (cAMP) formation and to increase guanosine cyclic monophosphate (cGMP) content in mouse ventricular myocardium. Hormone-induced inhibition of adenylate cyclase, the enzyme that synthesizes cAMP, and the cGMP response to alpha adrenergic agonists are mediated by a guanine nucleotide binding protein (N) sensitive to pertussis toxin. To evaluate the involvement of N proteins in the action of halothane on cyclic nucleotides in the heart, mice were pretreated with pertussis toxin, 50 micrograms/kg, ip, 72 h prior to exposure to halothane, 1.2 vol%. Pretreatment with the toxin decreased the cGMP response to halothane by 65% but was without effect on the decrease in myocardial cAMP induced by the anesthetic. The results indicate that a functionally active pertussis toxin-sensitive N protein is involved in the cGMP response to halothane, but not in the cAMP response.
Vulliemoz
Y
Y
Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
Verosky
M
M
D037361:Adenylate Cyclase Toxin; D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism*; D006221:Halothane / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism*; D037342:Pertussis Toxin; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D037361:Adenylate Cyclase Toxin; D010566:Virulence Factors, Bordetella; D000242:Cyclic AMP; D037342:Pertussis Toxin; D006152:Cyclic GMP; D006221:Halothane