Thiamylal and Thiopental Attenuate Beta-adrenergic Signaling Pathway by Suppressing Adenylyl Cyclase in Rat Ventricular Myocytes

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Title ( eng )
Thiamylal and Thiopental Attenuate Beta-adrenergic Signaling Pathway by Suppressing Adenylyl Cyclase in Rat Ventricular Myocytes
Creator
Hidaka Ikuhiro
Kurokawa Hiromi
Yuge Osafumi
Source Title
Hiroshima Journal of Medical Sciences
Volume 58
Issue 1
Start Page 9
End Page 15
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
The effects of intravenous anesthetics on myocytes have not been fully elucidated. To investigate the effects of various intravenous anesthetics such as fentanyl, morphine, ketamine, diazepam, midazolam, thiamylal, and thiopental on the beta-adrenergic signaling pathway, we measured isoproterenol-stimulated cyclic adenosine monophosphate (cAMP) production in freshly isolated rat ventricular myocytes. Fentanyl, morphine, ketamine, diazepam, and midazolam did not significantly affect isoproterenol-stimulated cAMP production. However, thiamylal and thiopental dose-dependently decreased cAMP production stimulated by isoproterenol or by forskolin, a direct adenylyl cyclase stimulator. In addition, we examined the role of protein kinase C (PKC) as a potential mediator of the thiamylal- or thiopentalinduced effects on cAMP production using bisindolylmaleimide I, a non-specific PKC inhibitor. Bisindolylmaleimide I did not alter the inhibitory effects of thiamylal or thiopental. Thiamylal and thiopental significantly decreased isoproterenol-stimulated cAMP production by suppressing the adenylyl cyclase. We conclude that barbiturates such as thiamylal and thiopental decrease isoproterenol-stimulated cAMP production by suppressing the adenylyl cyclase through PKC-independent mechanisms.
Keywords
Ventricular myocytes
Beta-adrenergic signaling pathway
Adenylyl cyclase
Barbiturates
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 2009-03
Rights
(c) Hiroshima University Medical Press.
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312