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(Circulation Research. 2001;88:9.)
© 2001 American Heart Association, Inc.

Reports

Reduction of [Ca²⁺]_i Restores Uncoupled ß-Adrenergic Signaling in Isolated Perfused Transgenic Mouse Hearts

Vladimir B. Serikov, Natalia N. Petrashevskaya, Amy M. Canning, Arnold Schwartz

From the Institute of Molecular Pharmacology and Biophysics (V.B.S., N.N.P., A.S.) and the Division of Cardiovascular Medicine, Department of Internal Medicine (A.M.C.), University of Cincinnati, College of Medicine, Cincinnati, Ohio.

Correspondence to Dr A. Schwartz, Director, Institute of Molecular Pharmacology and Biophysics, Cardiovascular Research Center, University of Cincinnati, 231 Bethesda Ave, Cincinnati, OH 45267-0828.

The effects of alterations in calcium in the perfusion media were studied on ß-adrenergic coupling in isolated hearts from 3 different transgenic mice: cardiac-specific overexpressed ₁ subunit of L-type calcium channel, overexpressed G_q, and phospholamban knockout. Isolated hearts from all 3 models, when studied at [Ca²⁺] of 2 mmol/L in the perfusate, showed the usual blunted or no response to ß-adrenergic stimulation. Lowering [Ca²⁺] to 0.75 to 1.5 mmol/L unloaded the hearts of calcium and restored to nearly normal the responsiveness to ß-agonist stimulation.

Key Words: calcium • adenylyl cyclase • cardiac hypertrophy

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