Role of NPR-C receptor on the activation of nitric oxide synthase induced by atrial natriuretic peptide in heart, aorta artery and kidney

pp 102-106

Abstract

In previous studies we demonstrated that nitric oxide synthase (NOS) activation would mediate, at least in part, the hypotensive, diuretic and natriuretic effects of atrial natriuretic peptide (ANP).

The aim of the present study was to investigate the natriuretic receptor and the signaling pathway pathway involve in NOS activation induced by ANP.

Wistar male rats were decapitated, and atria, aorta and kidney were extracted. Tissues NOS activity (pmol L-[U14C] citrulline/g tissue) were measured with L-[U14C] arginine as substrate. Both ANP and cANP (4-23) (NPR-C specific agonist) increased NOS activity in the studies tissues. ANP induced a higher increase in kidney and aorta than the increase observed with cANP. Theses effects were blocked by nifedipine (L-type Ca²⁺ channles blockers). Gi_1-2 protein inhibition with Pertussis Toxin blocked cANP effect on NOS activity in atria, aorta and kidney. 

NOS activation induced by ANP in atria would be due to an interaction between the peptide and the NPR-C receptor. Meanwhile this action would also involved NPR-A and/or NPR-B in aorta and kidney. ANP would interact with NPR-C receptor coupled to Gi protein, activating Ca²⁺ dependent NOS.