C-type natriuretic peptide (CNP), secreted from endothelial cells, dilates the vessel and increases the renal excretion of sodium and water. Plasma CNP level is not elevated in patients with congestive heart failure (CHF), but the myocardial content of CNP is increased, suggesting paracrine or autocrine role of CNP. We studied to compare the effect of ANP and CNP on vasorelaxation in CHF rat model.

Coronary artery ligation was performed in Sprague Dawley rats, resulting in CHF (n=5) and they were fed with ordinary chow for 10 weeks. After measuring hemodynamics, aorta and pulmonary artery were incised and studied in organ chamber to measure the isotonic force to KCl and to observe the relaxation response to atrial natriuretic peptide (ANP), and CNP in vessels precontracted with phenylephrine. Normal Sprague Dawley rats (n=5) were used as control.

There were no difference in vasorelaxation responses to ANP between control and CHF rats. The response to CNP was significantly impaired in both aorta and pulmonary artery of CHF rats compared to control rats. Maximal response to CNP in aorta was - 25.3±5.0% in CHF rats, - 74.7±16.0% in control rats. Maximal response to CNP in pulmonary artery was - 41.1±4.5% in CHF rats, - 79.2±9.3% in control rats.

The relaxation response to CNP was impaired in both aorta and pulmonary artery of CHF rats compared with control. These data suggest the differential regulation of natriuretic peptides (CNP and ANP) and their receptors in CHF rats.