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Inhibition of L-type Ca²⁺ current by C-type natriuretic peptide in bullfrog atrial myocytes: an NPR-C-mediated effect

¹Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and ²Department of Bioengineering, University of California, San Diego, La Jolla, California 92093-0412

Submitted 25 April 2003 ; accepted in final form 23 July 2003

Single atrial myocytes were isolated from the bullfrog heart and studied under current and voltage clamp conditions to determine the electrophysiological effects of the C-type natriuretic peptide (CNP). CNP (10^–8 M) significantly shortened the action potential and reduced its peak amplitude after the application of isoproteronol (10^–7 M). In voltage clamp studies, CNP inhibited isoproteronol-stimulated L-type Ca²⁺ current (I_Ca) without any significant effect on the inward rectifier K⁺ 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 I_Ca. Inclusion of cAMP in the recording pipette to stimulate I_Ca at a point downstream from adenylyl cyclase increased I_Ca, but this effect was not inhibited by cANF. These results provide the first demonstration that CNP can inhibit I_Ca 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.

action potential; C receptor; heart

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