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The mechanism of the diminished inotropic response to β-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 Ca 2+  concentration ([Ca 2+ ] i ) transients produced by isoproterenol were markedly diminished in diabetic myocytes. The inotropic and [Ca 2+ ] 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 Ca 2+  current ( I  Ca ) between control and diabetic myocytes. The rise of [Ca 2+ ] i in response to rapid caffeine application, an index of sarcoplasmic reticulum (SR) Ca 2+  content, was significantly decreased in diabetic myocytes. Isoproterenol, forskolin, and DBcAMP enhanced this [Ca 2+ ] 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 [Ca 2+ ] i responses of cardiac myocytes when stimulated at both β-adrenoceptors and the postreceptor level without affecting the I  Ca  response and 2) altered SR functions of uptake and/or release of Ca 2+  may primarily contribute to the diminished β-adrenergic response.

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

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