Abstract
The administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg s.c.) concurrently with Escherichia coli endotoxin (3 mg/kg i.v.) increased vascular permeability and caused mucosal damage in the rat intestine 1 h later. The vasopressin V1 receptor antagonist, [Mca1,Tyr(Me)2, Arg8]vasopressin (0.01-0.2 microgram/kg s.c., 15 min before endotoxin) dose-dependently reduced this damage. These results suggest a beneficial role of NO, counteracting the injurious vascular actions of endogenous vasopressin, in maintaining intestinal mucosal integrity in acute endotoxaemic states.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Antidiuretic Hormone Receptor Antagonists
-
Arginine / administration & dosage
-
Arginine / analogs & derivatives*
-
Arginine / toxicity
-
Arginine Vasopressin / analogs & derivatives*
-
Arginine Vasopressin / pharmacology
-
Capillary Permeability / drug effects*
-
Colon / drug effects
-
Dose-Response Relationship, Drug
-
Drug Synergism
-
Endotoxins / administration & dosage
-
Endotoxins / toxicity*
-
Escherichia coli / metabolism
-
Humans
-
Ileum / drug effects
-
Injections, Intravenous
-
Injections, Subcutaneous
-
Intestinal Mucosa / blood supply*
-
Intestinal Mucosa / drug effects
-
Male
-
Microcirculation / drug effects
-
NG-Nitroarginine Methyl Ester
-
Nitric Oxide / antagonists & inhibitors
-
Nitric Oxide / physiology*
-
Rats
-
Rats, Wistar
-
Vasopressins / metabolism
-
Vasopressins / pharmacology
Substances
-
Antidiuretic Hormone Receptor Antagonists
-
Endotoxins
-
vasopressin, 1-(2-mercapto-2,2-(cyclopentamethylene)propionic acid)-2-(O-methyl)Tyr-8-Arg-
-
Vasopressins
-
Arginine Vasopressin
-
Nitric Oxide
-
Arginine
-
NG-Nitroarginine Methyl Ester