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Am J Physiol Heart Circ Physiol 278: H1-H7, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 1, H1-H7, January 2000

Phosphatase inhibitor cantharidin blocks adenosine A1 receptor anti-adrenergic effect in rat cardiac myocytes

Prakash Narayan, Robert M. Mentzer Jr., and Robert D. Lasley

Department of Surgery, University of Kentucky College of Medicine, Lexington, Kentucky 40536

Experiments were performed to examine whether the protein phosphatase inhibitor cantharidin blocks the anti-adrenergic effect of adenosine A1 receptor stimulation. In electrically stimulated adult rat ventricular myocytes loaded with the intracellular calcium concentration ([Ca2+]i) indicator fluo-3, isoproterenol (10 nM) increased systolic [Ca2+]i by 46%, increased twitch amplitude by 56%, and increased total cellular cAMP content by 140%. The adenosine A1 receptor agonist 2-chloro-N6-cyclopentlyadenosine (CCPA) reduced isoproterenol-stimulated [Ca2+]i and contractility by 87 and 80%, respectively, but reduced cAMP content by only 18%. Cantharidin had no effects on myocyte [Ca2+]i, contractility, or cAMP in the absence or presence of isoproterenol but blocked the effects of CCPA on [Ca2+]i and contractility by ~44%. Cantharidin had no effect on CCPA attenuation of isoproterenol-induced increases in cAMP. Pretreatment with CCPA also reduced the increase in contractile parameters produced by the direct cAMP-dependent protein kinase A (PKA) activator 8-bromocAMP. These results suggest that activation of protein phosphatases mediate, in part, the anti-adrenergic effect of adenosine A1 receptor activation in ventricular myocardium.

calcium; contractility; adenosine 3',5'-cyclic monophosphate


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