L-ARGININE-RELATED RESPONSES TO PRESSURE AND VASOACTIVE AGENTS IN MONOCROTALINE-TREATED RAT PULMONARY-ARTERIES

To determine whether altered NO production contributes to attenuated d istensibility (alpha), vasoreactivity, and acetylcholine (ACh) dilatio n in pulmonary arteries from monocrotaline (MCT)-treated rats (J. A. M adden, P. A. Keller, R. M. Effrosa, C. Sequitte, J. S. Choy, and A. D. Hacker. J. Appl. Physiol. 76: 1589-1593, 1994), intralobar and sidebr anch arteries from rats 21 days after MCT treatment were cannulated an d pressurized and their diameter changes in response to KCl, norepinep hrine, angiotensin II, and pressure were measured in the presence of N -omega-nitro-L-arginine (NLA) and L-arginine. NLA treatment decreased MCT artery diameters more than normal arteries (P < 0.05) and abolishe d ACh dilation in both. Agonist responses were greater in normal but n ot MCT arteries. The alpha increased in NLA-treated normal (P < 0.05) but not MCT arteries. After L-arginine, normal and MCT arteries return ed to control diameters and dilated to ACh. Agonist responses returned to control in normal but not MCT arteries. Normal but not MCT arterie s dilated in calcium-free solution (P < 0.05). These results suggest t hat pulmonary arteries from rats with MCT-induced pulmonary hypertensi on produce more NO than do pulmonary arteries; inhibiting NO does not increase contractility; and decreased vasoreactivity and alpha values are not due to smooth muscle cell tone but may be due to abnormal vasc ular remodeling.