title: The intercellular communication via nitric oxide and its regulation in coupling of cyclic GMP synthesis upon stimulation of muscarinic cholinergic receptors in rat superior cervical sympathetic ganglia.
abstract: Cyclic GMP (cGMP) production in rat superior cervical sympathetic ganglia (SCG) was markedly increased (ca. 7-9-fold) by the addition of either acetylcholine (ACh; 0.1 mM) or a muscarinic agonist, carbachol (Carb; 0.1 mM), in the presence of an inhibitor (3-isobutyl-1-methylxanthine) for cGMP hydrolytic enzyme during in vitro aerobic incubation at 37 degrees C for 5 min. The ACh-induced accumulation of cGMP in SCG was effectively blocked (-73%) by the further addition of atropine (10 microM), a muscarinic antagonist, whereas a nicotinic blocker, hexamethonium (10 microM) partially antagonized (-41%) this ACh stimulation. The inhibitory effect of hexamethonium on ACh-evoked ganglionic cGMP production was effectively augmented (-83%) by addition of NG-monomethyl-L-arginine (L-NMMA, 50 microM), a compound that inhibits nitric oxide (NO) synthesis from L-arginine. Comparable inhibition of cGMP formation was observed following application of L-NMMA to the SCG upon stimulation of Carb. In contrast, L-NMMA had no effect on the decreased level of ACh-evoked cGMP production caused by the muscarinic antagonist. The Carb-induced elevation of ganglionic cGMP synthesis was significantly reduced within 1 min of incubation in the medium containing hemoglobin (Hb; 20 microM), an agent that scavenges only the extracellular fraction of NO. Thereafter, the tissue cGMP formation attenuated to the control level by subsequent incubation for several minutes. Addition of protein kinase C (PKC) activator, 12-O-tetradecanoylphorbol 13-acetate (TPA; 1 microM) to the medium significantly decreased Carb-evoked cGMP synthesis (-61%) in SCG, whereas superoxide dismutase (SOD; 30 U/ml) only slightly suppressed the Carb stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Physiology, Fujita Health University School of Medicine, Aichi-ken, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ando
authors.forename: T
authors.initials: T
authors.lastname: Tatematsu
authors.forename: S
authors.initials: S
authors.lastname: Kunii
authors.forename: Y
authors.initials: Y
authors.lastname: Nagata
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001369:Axons / Q000502:physiology; D002217:Carbachol / Q000494:pharmacology; D002450:Cell Communication / Q000502:physiology*; D018680:Cholinergic Antagonists / Q000494:pharmacology; D006152:Cyclic GMP / Q000096:biosynthesis*; D003714:Denervation; D005260:Female; D006454:Hemoglobins / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D019001:Nitric Oxide Synthase; D051381:Rats; D017208:Rats, Wistar; D011950:Receptors, Cholinergic / Q000378:metabolism*; D017783:Superior Cervical Ganglion / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014268:Trifluoperazine / Q000494:pharmacology; D019323:omega-N-Methylarginine
chemical_list: D018680:Cholinergic Antagonists; D006454:Hemoglobins; D011950:Receptors, Cholinergic; D014268:Trifluoperazine; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D002217:Carbachol; D001120:Arginine; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D000594:Amino Acid Oxidoreductases; D006152:Cyclic GMP; D000109:Acetylcholine; D013755:Tetradecanoylphorbol Acetate