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J Biol Chem, Vol. 274, Issue 31, 21503-21506, July 30, 1999

COMMUNICATION
Cardiac-specific Overexpression of the ₁ Subunit of the L-type Voltage-dependent Ca²⁺ Channel in Transgenic Mice
LOSS OF ISOPROTERENOL-INDUCED CONTRACTION

James N. Muth^§, Hiroshi Yamaguchi, Gabor Mikala, Ingrid L. Grupp^¶, William Lewis, Heping Cheng^**, Long-Sheng Song^**, Edward G. Lakatta^**, Gyula Varadi^§, and Arnold Schwartz

From the  Institute of Molecular Pharmacology and Biophysics, Departments of ^§ Cell Biology, Neurobiology, and Anatomy,  Pathology and Laboratory Medicine, ^¶ Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267 and the ^** Laboratory of Cardiovascular Science, Gerontology Research Center, NIA, National Institutes of Health, Baltimore, Maryland 21224

The L-type voltage-dependent calcium channel (L-VDCC) regulates calcium influx in cardiac myocytes. Activation of the -adrenergic receptor (AR) pathway causes phosphorylation of the L-VDCC and that in turn increases Ca²⁺ influx. Targeted expression of the L-VDCC ₁ subunit in transgenic (Tg) mouse ventricles resulted in marked blunting of the AR pathway. Inotropic and lusitropic responses to isoproterenol and forskolin in Tg hearts were significantly reduced. Likewise, Ca²⁺ current augmentation induced by iso- proterenol and forskolin was markedly depressed in Tg cardiomyocytes. Despite no change in AR number, isoproterenol-stimulated adenylyl cyclase activity was absent in Tg membranes and NaF and forskolin responses were reduced. We postulate an important pathway for regulation of the AR by Ca²⁺ channels.

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Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.

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