title: Comparison of the effects of pancuronium and vecuronium in canine coronary and renal arteries.
abstract: BACKGROUND
  Pancuronium has sympathomimetic actions but does not change or lowers systemic blood pressure in some studies of anesthetized humans and dogs. The present study was done to determine the actions and mechanisms of action of pancuronium on coronary and renal arteries other than those as a sympathomimetic agent.
  
  
  METHODS
  Helical strips of coronary and renal arteries from mongrel dogs were suspended in oxygenated, warmed Ringer-Locke solution, and changes in the isometric tension were recorded. In some strips, transmural electrical stimulation (5 Hz for 40 s) was applied to activate perivascular adrenergic nerves.
  
  
  RESULTS
  Pancuronium (10[-7] to 10[-5] M) caused dose-dependent relaxation in coronary and renal arteries contracted with prostaglandin (PG) F2alpha, whereas no significant response was induced with vecuronium. The relaxation was endothelium independent and abolished by indomethacin or tranylcypromine, a PGI2 synthase inhibitor. Transmural electrical stimulation caused coronary arterial relaxation, which was augmented by pancuronium and vecuronium. Desipramine also increased the response, and additional potentiation of the response was not elicited by pancuronium and vecuronium. In renal arteries, electrical stimulation caused contraction, which was also augmented by pancuronium and vecuronium. With desipramine treatment, these muscle relaxants did not potentiate the response. Endothelium-dependent coronary arterial relaxation caused by bradykinin was not affected by pancuronium.
  
  
  CONCLUSIONS
  Pancuronium-induced relaxations in canine coronary and renal arteries appear to be mediated by PGI2 released from subendothelial tissues. Potentiations by pancuronium and vecuronium of the response to adrenergic nerve stimulation are expected to be due to an inhibition of the norepinephrine uptake but not to facilitated release of the amine.
authors.affiliation: Department of Anesthesiology, Shiga University of Medical Science, Seta, Otsu, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Sai
authors.forename: K
authors.initials: K
authors.lastname: Ayajiki
authors.forename: T
authors.initials: T
authors.lastname: Okamura
authors.forename: S
authors.initials: S
authors.lastname: Nosaka
authors.forename: N
authors.initials: N
authors.lastname: Toda
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004730:Endothelium, Vascular / Q000502:physiology; D011464:Epoprostenol / Q000378:metabolism; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D003473:Neuromuscular Nondepolarizing Agents / Q000494:pharmacology*; D010197:Pancuronium / Q000494:pharmacology*; D012077:Renal Artery / Q000187:drug effects* / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects*; D014673:Vecuronium Bromide / Q000494:pharmacology*
chemical_list: D003473:Neuromuscular Nondepolarizing Agents; D014673:Vecuronium Bromide; D011464:Epoprostenol; D010197:Pancuronium; D007213:Indomethacin