Cyclic 3',5'-guanosine monophosphate synthesis induced by atrial natriuretic peptide, C-type natriuretic peptide, and nitric oxide in the rat retina.

摘要

This study was undertaken to determine whether pathways exist in the rat retina for atrial natriuretic peptide (ANP)-, C-type natriuretic peptide (CNP)-, and nitric oxide (NO)- cyclic 3', 5'-guanosine monophosphate (cGMP). Exposure of the retina to ANP (10(-7) mol/L), CNP (10(-7) mol/L), S-nitroso-N-acetylpenicillamine (10(-5) mol/L, SNAP; a NO donor), A23187 (10(-5)mol/L; a Ca2+ ionophore), and carbachol (10(-3) mol/L) caused 1.45 approximately 1.67-fold increases in cGMP content (P < .01). The increase in cGMP content induced by A23187 was blocked by 2-4-carboxyphenyl . 4455-tetramethyl imidazoline 1-oxyl 3-oxide (10(-3) mol/ L, carboxy-PTIO; a NO scavenger). Both carboxy-PTIO (10(-3) mol/L) and NG-nitro-L-arginine (10(-3) mol/L, L-NNA: a NO synthase inhibitor) blocked the increase in cGMP content induced by carbachol. Atropine (10(-50 mol/L; a muscarinic receptor antagonist) also blocked the cGMP increase induced by carbachol. These data demonstrate that ANP-, CNP-, and NO-cGMP pathways exist in the rat retina and that the NO-cGMP pathway may be linked to the activation of the muscarinic receptor.