Abstract
Nitric oxide (NO) regulates pulmonary vascular tone and may play a role in neonatal pulmonary vascular remodeling. We investigated the role of exogenous and endogenous NO in regulating neonatal pulmonary artery smooth muscle cell(SMC) proliferation in vitro. The effect of exogenous NO was evaluated by a NO donor, S-nitroso-N-acetyl penicillamine(SNAP), and a NO scavenger, Carboxy-PTIO (CPTIO). Endogenous NO was evaluated by an inducible nitric oxide synthase (iNOS) inhibitor,S-(2-Aminoethyl)isothiourea (AETU), and iNOS stimulators, lipopolysaccharide(LPS) and interleukin-1β (IL1β). SMC plated with different additive dilutions were counted at 72 hours by Coulter counter. The effect of hypoxia on endogenous NO was evaluated by estimating cyclic GMP(cGMP) by ELISA in SMC exposed to 2, 7, and 20% O2 for 48 hours. SNAP inhibited SMC proliferation (p<0.005 by ANOVA) while CPTIO, AETU, LPS, and IL1β did not significantly alter SMC counts. Levels of cGMP were similar at different O2 levels (cGMP/106cells: 2%O2: 69±10pg; 7%: 52±6pg; 20%: 54±9pg). These results suggest that exogenous NO(e.g. endothelial derived) affects SMC proliferation but that iNOS probably does not modify SMC proliferation under basal conditions, during hypoxia, or by stimuli known to activate iNOS such as LPS and IL1β.Figure
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