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Articles in PresS, published online ahead of print January 31, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00988.2001
Submitted on November 13, 2001
Accepted on January 28, 2002
1 Neurobiology, Pharmacology, and Physiology, University of Chicago, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: ddoyle{at}hearts.bsd.uchicago.edu.
We have assessed the cellular localization and relative concentration of the C-type natriuretic peptide (CNP) guanylyl cyclase-B receptor in adult rat heart ventricle by several techniques. In frozen sections of ventricle anti-receptor antibody stained the vasculature and cells interstitial to myocytes but not myocytes themselves. The same antibody detected GC-B in immunoblots of protein extracts of non-myocytes, but not myocytes, and recognized an equivalent protein in extracts of cultured cardiac fibroblasts but not A7r5 rat smooth muscle cells. In functional assays, CNP-induced cGMP accumulation per mg. cell protein was an order of magnitude greater in cultured cardiac fibroblasts than in A7r5 smooth muscle cells and 2 orders of magnitude greater than in freshly isolated cardiac myocytes. Modulation of cGMP accumulation by phosphodiesterases (PDEs) was cell specific as determined by antagonist pharmacological profiles- PDE1 in fibroblasts, PDE2 in A7r5 cells, and PDE3 in myocytes, suggesting that the significant but low-level cGMP response to CNP measured in heart myocytes is not due to non-myocyte contamination. Fibroblasts of cardiac origin do not show an interactive relationship between receptor responsiveness to CNP, cGMP levels and proliferation-related mitogen-activated signal transduction pathways. While previous reports suggest CNP exerts significant effects in neonatal rat cardiomyocytes, our results suggest that fibroblasts are likely the most responsive cell type (in terms of cGMP production) in the adult rat heart.
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