title: Control of cardiovascular function in the icefish Chionodraco hamatus: involvement of serotonin and nitric oxide.
abstract: The involvement of nitric oxide (NO) in the branchial circulation and cardiac performance of the Antarctic hemoglobinless icefish Chionodraco hamatus was investigated using isolated and perfused head and working heart preparations. In the branchial vasculature under basal (i.e. unstimulated conditions), the nitric oxide synthase (NOS) inhibitor L-NIO (L-N(5)-(1-iminoethyl) ornithine, 10(-5) and 10(-4) M), caused a marked vasoconstriction (20%), indicating a basal nitrergic vasodilator tone, while the dose-response curve of the NO donor SIN-1 (3-morpholinosydnonimine) showed a dose-dependent vasodilator effect. Acetylcholine induced a dose-dependent branchial vasoconstriction mediated by muscarinic receptors, since the effects were abolished by pre-treatment with atropine (10(-4) M). Serotonin (5-HT) induced a dose-dependent branchial methysergide-sensitive vasoconstriction which was abolished by pre-treatment with L-NIO, indicating a NO-dependent mechanism. On the isolated heart, the NOS inhibitor L-NMMA (N(G)-monomethyl-L-arginine) 10(-4) M produced a small, but significant decrease of heart rate and, as a consequence, a decrease of power output, while the NO donor sodium nitroprusside (SNP) 10(-4) M elicited increases of stroke volume, stroke work and power output, suggesting an exogenous NO-dependent positive inotropism. Exposure of the bulbus arteriosus to L-NMMA was without any appreciable effect. In contrast, SNP produced a notable relaxation of the bulbus wall with a marked increase of its stiffness, as indicated by the increase of systolic and diastolic dP/dt max (23 and 104%, respectively).
authors.affiliation: Department of Cell Biology, University of Calabria, Arcavacata di Rende, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Pellegrino
authors.forename: R
authors.initials: R
authors.lastname: Acierno
authors.forename: B
authors.initials: B
authors.lastname: Tota
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage; D000818:Animals; D000864:Antarctic Regions; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005399:Fishes / Q000502:physiology*; D005880:Gills / Q000098:blood supply; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D008981:Molsidomine / Q000008:administration & dosage / Q000031:analogs & derivatives*; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000008:administration & dosage; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009952:Ornithine / Q000031:analogs & derivatives* / Q000494:pharmacology; D012701:Serotonin / Q000008:administration & dosage / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D012701:Serotonin; C065027:N(G)-iminoethylornithine; C002385:linsidomine; D008981:Molsidomine; D009952:Ornithine; D019001:Nitric Oxide Synthase; D000109:Acetylcholine