title: Adaptive vasodilatory response after octreotide treatment.
abstract: Despite the suppression of glucagon release, an adaptive response aimed at maintaining vasodilatation after octreotide treatment may exist in portal hypertension. The present study was undertaken to evaluate the possible interaction between endothelium and non-endothelium-derived vasodilators after 1-wk octreotide administration in cirrhotic rats. Rats were allocated to receive either vehicle or octreotide (30 or 100 microg/kg every 12 h subcutaneously). Hemodynamic values, plasma glucagon levels, endothelium-related vasodilatory activities, and aortic endothelial nitric oxide synthase (eNOS) expression were determined after treatment. Octreotide administration decreased plasma glucagon and increased serum 6-keto-PGF(1 alpha) and NOx levels without affecting the hemodynamic values. In cirrhotic rats receiving octreotide, there was a blunt response to either L-NAME or indomethacin administration alone, but this blunt pressor response disappeared after simultaneous administration of the two drugs. Additionally, an increased aortic eNOS expression was observed in cirrhotic rats receiving 1-wk octreotide. It is concluded that 1-wk octreotide treatment did not correct the hemodynamic derangement in cirrhotic rats. The enhanced endothelium-related vasodilatory activity was noted after octreotide treatment that overcame the octreotide-induced hemodynamic effects in portal hypertension.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital and National Yang-Ming University School of Medicine, Taiwan.
authors.forename: Y Y
authors.initials: YY
authors.lastname: Yang
authors.forename: H C
authors.initials: HC
authors.lastname: Lin
authors.forename: Y T
authors.initials: YT
authors.lastname: Huang
authors.forename: T Y
authors.initials: TY
authors.lastname: Lee
authors.forename: W C
authors.initials: WC
authors.lastname: Lee
authors.forename: M C
authors.initials: MC
authors.lastname: Hou
authors.forename: F Y
authors.initials: FY
authors.lastname: Lee
authors.forename: F Y
authors.initials: FY
authors.lastname: Chang
authors.forename: S D
authors.initials: SD
authors.lastname: Lee
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001011:Aorta / Q000201:enzymology; D015153:Blotting, Western; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005934:Glucagon / Q000097:blood; D006975:Hypertension, Portal / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D008103:Liver Cirrhosis / Q000378:metabolism; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009566:Nitrates / Q000097:blood; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000032:analysis / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D009573:Nitrites / Q000097:blood; D015282:Octreotide / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013004:Somatostatin / Q000378:metabolism; D013152:Splanchnic Circulation / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology*
chemical_list: D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D009566:Nitrates; D009573:Nitrites; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D013004:Somatostatin; D015121:6-Ketoprostaglandin F1 alpha; D005934:Glucagon; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D015282:Octreotide; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin