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Am J Physiol Heart Circ Physiol 274: H1849-H1857, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 6, H1849-H1857, June 1998

Effects of beta -adrenoceptor stimulation on contractility, [Ca2+]i, and Ca2+ current in diabetic rat cardiomyocytes

Atsushi Tamada, Yuichi Hattori, Hideki Houzen, Yoichi Yamada, Ichiro Sakuma, Akira Kitabatake, and Morio Kanno

Departments of Pharmacology and Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo 060, Japan

The mechanism of the diminished inotropic response to beta -adrenoceptor stimulation in diabetic hearts was studied in enzymatically isolated diabetic rat ventricular myocytes in comparison with age-matched controls. The increases in contractions and intracellular Ca2+ concentration ([Ca2+]i) transients produced by isoproterenol were markedly diminished in diabetic myocytes. The inotropic and [Ca2+]i responses to forskolin and dibutyryl cAMP (DBcAMP) were also reduced. No significant difference was found in the stimulating effects of isoproterenol, forskolin, and DBcAMP on the L-type Ca2+ current (ICa) between control and diabetic myocytes. The rise of [Ca2+]i in response to rapid caffeine application, an index of sarcoplasmic reticulum (SR) Ca2+ content, was significantly decreased in diabetic myocytes. Isoproterenol, forskolin, and DBcAMP enhanced this [Ca2+]i response to caffeine in control myocytes more markedly than in diabetic myocytes. The changes in the isoproterenol responses observed in diabetic myocytes were prevented by insulin therapy. We conclude that 1) diabetes causes an impairment of the contractile and [Ca2+]i responses of cardiac myocytes when stimulated at both beta -adrenoceptors and the postreceptor level without affecting the ICa response and 2) altered SR functions of uptake and/or release of Ca2+ may primarily contribute to the diminished beta -adrenergic response.

diabetes mellitus; cell shortening; calcium transient; indo 1; L-type calcium channel; sarcoplasmic reticulum


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