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Glucagon-induced densensitization: correlation between cyclic AMP levels and contractile force.

L F Yao, K M MacLeod, J H McNeill

European Journal of Pharmacology

|April 8, 1982

Summary

Glucagon desensitization in guinea pig atria reduces its inotropic effects and cyclic AMP elevation. Contractile force strongly correlates with cyclic AMP levels, even after desensitization.

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Area of Science:

Pharmacology
Cardiovascular Physiology
Molecular Biology

Background:

Glucagon exerts inotropic effects on cardiac tissue.
The role of cyclic AMP in glucagon's cardiac actions is established.
Understanding desensitization mechanisms is crucial for therapeutic applications.

Purpose of the Study:

To investigate the in vitro desensitization of guinea pig left atria to glucagon.
To determine the relationship between glucagon's inotropic effect and cyclic AMP levels during desensitization.

Main Methods:

In vitro treatment of guinea pig left atria with 10(-6) M glucagon.
Measurement of contractile force and cyclic AMP levels before and after glucagon exposure.
Comparison of responses in control and glucagon-desensitized atria.

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Main Results:

Glucagon desensitization was successfully induced in vitro.
Desensitized atria showed a diminished contractile response to glucagon.
The ability of glucagon to increase cyclic AMP levels was lost in desensitized atria.
A significant positive correlation existed between contractile force and cyclic AMP levels.

Conclusions:

Glucagon desensitization involves impaired cyclic AMP signaling.
The inotropic effects of glucagon are closely linked to cyclic AMP elevation.
This study provides insights into the molecular mechanisms of cardiac desensitization.