Despite the suppression of glucagon release, an adaptive response aimed at
maintaining vasodilatation after octreotide treatment may exist in portal h
ypertension. The present study was undertaken to evaluate the possible inte
raction between endothelium and non-endothelium-derived vasodilators after
1-wk octreotide administration in cirrhotic rats. Rats were allocated to re
ceive either vehicle or octreotide (30 or 100 mug/kg every 12 h subcutaneou
sly). Hemodynamic values, plasma glucagon levels, endothelium-related vasod
ilatory activities, and aortic endothelial nitric oxide synthase (eNOS) exp
ression were determined after treatment. Octreotide administration decrease
d plasma glucagon and increased serum 6-keto-PGF(1 alpha) and NOx levels wi
thout affecting the hemodynamic values. In cirrhotic rats receiving octreot
ide, there was a blunt response to either L-NAME or indomethacin administra
tion alone, but this blunt pressor response disappeared after simultaneous
administration of the two drugs. Additionally, an increased aortic eNOS exp
ression was observed in cirrhotic rats receiving 1-wk octreotide. It is con
cluded that 1-wk octreotide treatment did not correct the hemodynamic deran
gement in cirrhotic rats. The enhanced endothelium-related vasodilatory act
ivity was noted after octreotide treatment that overcame the octreotide-ind
uced hemodynamic effects in portal hypertension.