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PMID: 10645897 Published · ppublish English Journal Article

Role of neuronal nitric oxide synthase in regulation of vascular and ductus arteriosus tone in the ovine fetus.

American journal of physiology. Lung cellular and molecular physiology ·Vol. 278 ·No. 1 ·2000-01-00 ·Pages L105-10

Rairigh RL, Storme L, Parker TA, Le Cras TD, Markham N, Jakkula M, Abman SH

Abstract

Nitric oxide (NO) is produced by NO synthase (NOS) and contributes to the regulation of vascular tone in the perinatal lung. Although the neuronal or type I NOS (NOS I) isoform has been identified in the fetal lung, it is not known whether NO produced by the NOS I isoform plays a role in fetal pulmonary vasoregulation. To study the potential contribution of NOS I in the regulation of basal fetal pulmonary vascular resistance (PVR), we studied the hemodynamic effects of a selective NOS I antagonist, 7-nitroindazole (7-NINA), and a nonselective NOS antagonist, N-nitro-L-arginine (L-NNA), in chronically prepared fetal lambs (mean age 128 +/- 3 days, term 147 days). Brief intrapulmonary infusions of 7-NINA (1 mg) increased basal PVR by 37% (P < 0.05). The maximum increase in PVR occurred within 20 min after infusion, and PVR remained elevated for up to 60 min. Treatment with 7-NINA also increased the pressure gradient between the pulmonary artery and aorta, suggesting constriction of the ductus arteriosus (DA). To test whether 7-NINA treatment selectively inhibits the NOS I isoform, we studied the effects of 7-NINA and L-NNA on acetylcholine-induced pulmonary vasodilation. The vasodilator response to acetylcholine remained intact after treatment with 7-NINA but was completely inhibited after L-NNA, suggesting minimal effects on endothelial or type III NOS after 7-NINA infusion. Western blot analysis detected NOS I protein in the fetal lung and great vessels including the DA. NOS I protein was detected in intact and endothelium-denuded vessels, suggesting that NOS I is present in the medial or adventitial layer. We conclude that 7-NINA, a selective NOS I antagonist, increases basal PVR, systemic arterial pressure, and DA tone in the late-gestation fetus and that NOS I protein is present in the fetal lung and great vessels. We speculate that NOS I may contribute to NO production in the regulation of basal vascular tone in the pulmonary and systemic circulations and the DA.

MeSH Terms
Acetylcholine/pharmacology Animals Blotting, Western Ductus Arteriosus/physiology Enzyme Inhibitors/pharmacology Fetus/metabolism,physiology Gestational Age Hemodynamics/drug effects Indazoles/pharmacology Nitric Oxide Synthase/antagonists & inhibitors,metabolism,physiology Nitric Oxide Synthase Type I Nitroarginine/pharmacology Pulmonary Circulation/drug effects Sheep Vasodilation/drug effects Vasomotor System/physiology
Chemicals
Enzyme Inhibitors Indazoles Nitroarginine Nitric Oxide Synthase Nitric Oxide Synthase Type I Acetylcholine 7-nitroindazole
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Rairigh R L
Pediatric Heart Lung Center, Department of Pediatrics, University of Colorado School of Medicine, Denver, Colorado 80218-1088, USA.
Storme L
Parker T A
Le Cras T D
Markham N
Jakkula M
Abman S H
Article Info
Journal
American journal of physiology. Lung cellular and molecular physiology
Abbr.
Am J Physiol Lung Cell Mol Physiol
ISSN
1040-0605
Published
2000-01-00
Pages
L105-10
Language
English
Region
United States
NLM ID
100901229
Subset
IM
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