SEGMENTAL HETEROGENEITY OF NO-MEDIATED PULMONARY VASODILATION IN RATS

Nitric oxide (NO) is known to elicit vasodilation in the preconstricte d rat lung. However, the sites of dilation within the pulmonary vascul ature remain unknown. We hypothesized that donated NO would dilate all areas of constriction within the pulmonary vasculature, whereas recep tor-mediated, NO-induced dilations would correspond to regional bindin g of agents. Isolated lungs from male Sprague-Dawley rats were perfuse d at constant flow with physiological saline solution. Pulmonary arter ial and pulmonary venous pressures were monitored, while pulmonary mic rovascular pressures were estimated by vascular occlusion. Lungs were constricted with U-46619, and upon development of a stable degree of v asoconstriction, the NO donor sodium nitroprusside or the endothelium- dependent dilators A23187, arginine vasopressin, or ATP were administe red. U-46619 caused constriction of both arterial and venous segments. Administration of sodium nitroprusside and the calcium ionophore A231 87 elicited similar dilation of preconstricted arterial and venous seg ments. Arginine vasopressin significantly dilated both arterial and ve nous segments, with a greater reversal of venous resistance. In contra st, ATP significantly reduced arterial resistance more than venous. Th ese results demonstrate that donated NO uniformly dilates all constric ted regions of the pulmonary vasculature. However, receptor-mediated, endothehum-dependent dilators display characteristic heterogeneities i n the sites of decreased pulmonary vascular resistance.