Response of normoxic pulmonary arteries of the rat in the resting and contracted state to NO synthase blockade

Abstract

1. The pulmonary vasculature is normally in a low resting state of tone. It has been hypothesized that this basal tone is actively maintained by the continuous release of a vasodilator in the resting state. However, evidence for basal release of nitric oxide (NO) is inconclusive. 2. We studied the release of NO in arteries from the pulmonary circulation of male Wistar-Kyoto rats by examining the effects of the L-arginine analogue N(G)-nitro-L-arginine methyl ester (L-NAME) on resting pulmonary arteries and on vessels pre-contracted with prostaglandin F(2α) (PGF(2α)). 3. Rats (n = 21) were killed by an overdose with pentobarbitone. Pulmonary arteries were dissected (mean internal diameter 459 ± 11 μm) and mounted in a small vessel wire myograph. Resting tensions were set to simulate transmural pressures of 17.5 mmHg. 4. L-NAME (100 μM) was found to produce a contraction of 0.64 ± 0.09 mN mm in resting pulmonary arteries when added alone to the myograph bath. This contraction was not produced following removal of the endothelium. Vessel contraction to PGF(2α) (100 μM) was found to be significantly greater when carried out in the presence of L-NAME (100 μM) - 1.37 ± 0.15 mN mm-1 compared with 1.96 ± 0.17 mN mm-1. Dilatation following acetylcholine (ACh) (1 μM) was abolished in the presence of L-NAME (100 μM). 5. Rat pulmonary artery contraction in response to the addition of L-NAME and the absence of contraction upon removal of the endothelium provides supportive evidence of the active release of nitric oxide for the maintenance of resting tone.