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Am J Physiol Heart Circ Physiol (July 24, 2003). doi:10.1152/ajpheart.00388.2003
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Submitted on April 25, 2003
Accepted on July 23, 2003

Inhibition of L-type Calcium Current by C-type Natriuretic Peptide In Bullfrog Atrial Myocytes: An NPR-C Mediated Effect

Robert A. Rose1*, Alan E. Lomax1, and Wayne R. Giles1

1 Department of Phyisiology and Biophysics, University of Calgary, Calgary, Alberta, Canada

* To whom correspondence should be addressed. E-mail: rarose{at}ucalgary.ca.

Single atrial myocytes were isolated from the bullfrog heart and studied under current and voltage clamp conditions to determine the electrophysiological effects of C-type natriuretic peptide, CNP. CNP (10-8 M) significantly shortened the action potential and reduced its peak amplitude following the application of isoproteronol (10-7 M). In voltage clamp studies, CNP inhibited isoproteronol-stimulated L-type calcium current (ICa) without any significant effect on the inward rectifier potassium current. The effects of cANF (10-8 M), a selective agonist of the natriuretic peptide C receptor (NPR-C), were very similar to those of CNP. Moreover, HS-142-1, an antagonist of the guanylyl cyclase-linked NPR-A and NPR-B receptors did not alter the inhibitory effect of CNP on ICa. Inclusion of cAMP in the recording pipette to stimulate ICa at a point downstream from adenylyl cyclase, increased ICa, but this effect was not inhibited by cANF. These results provide the first demonstration that CNP can inhibit ICa after binding to NPR-C, and suggest that this inhibition involves a decrease in adenylyl cyclase activity, which leads to reduced intracellular levels of cAMP.




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