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Halothane interaction with guanine nucleotide binding proteins in mouse heart.

Y Vulliemoz¹, M Verosky

¹Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032.

|December 1, 1988

Summary

Pertussis toxin blocks halothane

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Area of Science:

Cardiovascular Physiology
Anesthesiology
Molecular Pharmacology

Background:

Volatile anesthetics affect cardiac cyclic nucleotide levels.
Adenosine cyclic monophosphate (cAMP) and guanosine cyclic monophosphate (cGMP) are key intracellular messengers.
Guanine nucleotide-binding proteins (N proteins) mediate cellular responses to hormones and anesthetics.

Purpose of the Study:

To investigate the role of pertussis toxin-sensitive N proteins in mediating the effects of halothane on cardiac cyclic nucleotides.
To determine if N proteins are involved in halothane-induced changes in cAMP and cGMP levels in mouse ventricular myocardium.

Main Methods:

Mice were pretreated with pertussis toxin.
Animals were subsequently exposed to halothane (1.2 vol%).
Cardiac cAMP and cGMP levels were measured to assess the impact of halothane and pertussis toxin.

Main Results:

Pertussis toxin pretreatment significantly reduced the increase in cardiac cGMP content induced by halothane by 65%.
Pertussis toxin did not affect the decrease in cardiac cAMP formation caused by halothane.
This suggests a specific role for N proteins in the cGMP pathway.

Conclusions:

A pertussis toxin-sensitive N protein mediates the halothane-induced increase in cardiac cGMP.
The cAMP response to halothane in the heart is not mediated by this specific N protein.
These findings elucidate the molecular mechanisms underlying anesthetic actions on cardiac signaling pathways.

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