title: Cardiovascular actions of frog urotensin II in the frog, Rana catesbeiana.
abstract: The effects of synthetic frog urotensin II on cardiac output and arterial blood pressure and on the motility of isolated vascular smooth muscle were investigated in the bullfrog, Rana catesbeiana. Bolus injections of frog urotensin II (100 nmol/kg) into the left systemic arch produced a rapid and sustained fall in blood flow through the right branch of the truncus arteriosus (to 62 +/- 5% of preinjection values; n = 8). The response exhibited strong tachyphylaxis. There were no significant effects on heart rate and central arterial blood pressure but the fact that a fall in cardiac output was not accompanied by a fall in pressure suggests that the peptide produced an increase in peripheral vascular resistance. Rings of vascular smooth muscle from the proximal and distal regions of the left and right systemic arches responded to urotensin II with sustained and concentration-dependent contractions. The tissues from the different regions did not significantly differ in their maximum response and sensitivity to the peptide (EC50 values from 4.6 x 10(-9) to 6.5 x 10(-9) M; n = 6). Acetylcholine (3 x 10(-8) to 3 x 10(-6) M) significantly (P < 0.05) relaxed the rings in an endothelium-dependent manner but urotensin II did not produce relaxation at any concentration tested. The contractile effect of urotensin II (10(-7) M) was not affected by preincubation of the rings with atropine, tetrodotoxin, and somatostatin-14 but indomethacin produced a significant (P < 0.05) decrease in the amplitude of the contractions of the systemic arch (to 18 +/- 2% of control values; n = 6). Arachidonic acid (10(-5) M) also produced a sustained contraction of the rings. The data suggest an involvement of prostaglandin synthesis in the contractile action of urotensin II on isolated frog vascular smooth muscle but, unlike in mammals, urotensin II does not stimulate nitric oxide synthesis in this tissue.
authors.affiliation: Department of Biomedical Sciences, Creighton University Medical School, Omaha, Nebraska 68178.
authors.forename: K
authors.initials: K
authors.lastname: Yano
authors.forename: J W
authors.initials: JW
authors.lastname: Hicks
authors.forename: H
authors.initials: H
authors.lastname: Vaudry
authors.forename: J M
authors.initials: JM
authors.lastname: Conlon
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D011892:Rana catesbeiana; D013004:Somatostatin / Q000494:pharmacology; D013045:Species Specificity; D013779:Tetrodotoxin / Q000494:pharmacology; D014579:Urotensins / Q000494:pharmacology*
chemical_list: D014579:Urotensins; D016718:Arachidonic Acid; D013779:Tetrodotoxin; D013004:Somatostatin; D001285:Atropine; C029677:urotensin II; D000109:Acetylcholine; D007213:Indomethacin