ORALLY-ADMINISTERED L-ARGININE DOES NOT ALTER RIGHT-VENTRICULAR HYPERTROPHY IN CHRONICALLY HYPOXIC RATS

Evidence suggests that nitric oxide synthesis within the pulmonary cir culation may be attenuated during chronic hypoxia in Wistar rats due t o reduced L-arginine availability. In contrast, chronically hypoxic Sp rague-Dawley rats exhibit normal endothelium-dependent pulmonary vasod ilation. The purpose of the present study was to determine whether 1) Wistar rats demonstrate greater right ventricular (RV) hypertrophy in response to chronic hypoxia than Sprague-Dawley rats and 2) chronic ad ministration of L-arginine would diminish this response in Wistar rats . L-Arginine had no effect on the degree of hypoxia-induced RV hypertr ophy or polycythemia in either strain of rat. However, Wistar rats dem onstrated greater hypoxia-induced RV hypertrophy and polycythemia comp ared with Sprague-Dawley rats. To determine whether chronically hypoxi c Wistar rats indeed exhibit impaired endothelium-dependent pulmonary vasodilation, isolated lungs from control and chronically hypoxic Wist ar rats were administered the endothelium-dependent pulmonary vasodila tors A23187 or vasopressin. Vasodilatory responses to either agent wer e unaffected by chronic hypoxic exposure. We conclude that endothelium -dependent pulmonary vasodilation is maintained in the pulmonary circu lation of chronically hypoxic Wistar and Sprague-Dawley rats.