calcimycin and 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole

This study was undertaken to determine whether atrial natriuretic peptide (ANP)-, C-type natriuretic peptide (CNP)-, and nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathways exist in the rat retina. Exposure of the retina to ANP (10(-7)M), CNP (10(-7)M), S-nitroso-N-acetylpenicillamine (10(-5)M, SNAP; a NO doner), A23187 (10(-5)M; a Ca2+ionophore), and carbachol (10(-5)M) caused 1.45-1.67 fold increases in cGMP content (p < 0.01). Carboxy-PTIO (10(-3)M; a NO scavanger) blocked the increase in cGMP induced by A23187. Both carboxy-PTIO (10(-3)M) and NG-nitro-L-arginine (10(-3)M, L-NNA; a NO inhibitor) blocked the increase in cGMP induced by carbachol. Atropine (10(-5)M; 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 retina and that the NO-cGMP pathway may be linked to the activation of the muscarinic receptor.

Topics: Animals; Atrial Natriuretic Factor; Atropine; Benzoates; Calcimycin; Carbachol; Cyclic GMP; Imidazoles; In Vitro Techniques; Ionophores; Male; Natriuretic Peptide, C-Type; Nitric Oxide; Nitroarginine; Penicillamine; Proteins; Rats; Rats, Wistar; Retina; S-Nitroso-N-Acetylpenicillamine