Objective: To investigate the mechanism of vasodilatory effects of C-type natriuretic peptide (CNP).
Methods: Tension changes in aortic rings of rabbits were recorded with the presence of CNP or C-type natriuretic peptide receptor (NPR-C) agonist (cANF4-23) after pretreatment with epinephrine (NE) or 60 mmol/L KCl. The vasodilatory effects of four types of potassium channel blocker and NPR-C antagonist (cANF4-28) were also tested.
Results: A maximal vasorelaxant effects of (33.5 +/- 5.9) % and (38.4 +/- 10.6)% were recorded in the presence of 1 micromol/L CNP and cANF4-23, respectively, cANF4-28 attenuated the action of CNP [(19.8 +/- 8.3)%]. The vasorelaxant effects of CNP and cANF4-23 decreased significantly after pretreatment with 60 mmol/L KCl (P < 0.01). Glibenclamide and BaCl2 also attenuated the relaxant activities of CNP (P < 0.05). But only BaClZ decreased the vasodilatory action of cANF4-23 (P < 0.05).
Conclusion: The relaxant activity of CNP is mediated through three paths: NPR-B/KATP, NPR-C/KIR and NPR-C/calcium channels.