| Research Abstract |
The effects of vasopressin on contraction were studied in normal and endotoxin-treated human gastroepiploic arterial rings in vitro. In this tissue, vasopressin (50-500 pg/mL) produced concentration-dependent, endothelium-independent contractions. Vasopressin also enhanced the contraction elicited by 1.0 muM norepinephrine (NE) both in the presence and absence of endothelium. Endotoxin (10 mug/mL) attenuated 1 .0 muM NE-induced contractions and this attenuation was reversed by 300 muM N^G-nitro-L-arginine-methyl ester (L-NAME) or 300 muM N^G-nitro-L-arginine (L-NoArg). After 12 hours' treatment of endotoxin, vasopressin-induced contraction was attenuated and amplifying effect of vasopressin was diminished. However, the amplifying effect was stronger than the contractile effect of vasopressin. 1.0 muM beta-Mercapto-[beta, beta-cyclopentamethyllenpropionyl 1, O-MeTyr2, Arg8]-vasopressin (antagonist of vasopressin Vi receptor ) and 1.0 iotaM des-Gly9-[beta-Mercapto-"b, beta-cyclopentametylenepropionyl 1 , O-MeTyr^2, Arg^8] -vasopressin (antagonist of V_1-V_2 vasopressin receptor ) both diminished these vascular reactions induced by vasopressin. Implication : These results suggest that vasopressin, in addition to its direct vasoconstrictor effect, strongly enhances the responses to NE through V_1-receptor stimulation and that the role of vasopressin in the management of endotoxin-induced vasodilation will be important.
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