Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma.

Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Research Abstract Details 

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Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Abstract Text:

Ramadan B Sopi,Musa A Haxhiu,Richard J Martin,Ismail A Dreshaj,Suneel Kamath,Syed I A Zaidi,Ramadan B Sopi,Musa A Haxhiu,Richard J Martin,Ismail A Dreshaj,Suneel Kamath,Syed I A Zaidi,

Exposure of immature lungs to hyperoxia for prolonged periods contributes to neonatal lung injury and airway hyperreactivity. We studied the role of disrupted nitric oxide-guanosine 3',5'-cyclic monophosphate (NO-cGMP) signaling in impairing the relaxant responses of lung tissue from hyperoxia-exposed rat pups. Pups were exposed to >/=95% O(2) or room air for 7 days starting from days 1, 5, or 14. The animals were killed, lungs were removed, and 1-mm-thick lung parenchymal strips were prepared. Lung parenchymal strips of room air or hyperoxic pups were preconstricted using bethanechol and then graded electrical field stimulation (EFS) was applied to induce relaxation. EFS-induced relaxation of lung parenchymal strips was greater at 7 and 12 days than at 21 days in room air-exposed rat pups. Hyperoxic exposure significantly reduced relaxation at 7 and 12 days but not 21 days compared with room air exposure. NO synthase blockade with N(omega)-nitro-l-arginine methyl ester diminished relaxant responses in room air but not in hyperoxic pups at 12 days. After incubation with supplemental l-arginine, the relaxation response of hyperoxic strips was restored. cGMP, a key mediator of the NO signaling pathway, also decreased in strips from hyperoxic vs. room air pups and cGMP levels were restored after incubation with supplemental l-arginine. In addition, arginase activity was significantly increased in hyperoxic lung parenchymal strips compared with room air lung parenchymal strips. These data demonstrate disruption of NO-cGMP signaling in neonatal rat pups exposed to hyperoxia and show that bioavailability of the substrate l-arginine is implicated in the predisposition of this model to airway hyperreactivity.

Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Publishing Authors By Initials

RB Sopi,MA Haxhiu,RJ Martin,IA Dreshaj,S Kamath,SI Zaidi,RB Sopi,MA Haxhiu,RJ Martin,IA Dreshaj,S Kamath,SI Zaidi,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Lung cellular and

VOLUME: 293

Page Numbers: L1029-36

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 27

MONTH: 07

YEAR: 2007

Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901229

Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: antagonists & inhibitors

Chemical & Substance for Abstract: Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma. Information

Substance Name: Arginase

Registry Number: EC 3.5.3.1

Grant and Affiliation Information for Disruption of NO-cGMP signaling by neonatal hyperoxia impairs relaxation of lung parenchyma.

AFFILIATION: Dept. of Pediatrics, Rainbow Babies and Children Hospital, Case Western Reserve Univ., 11100 Euclid Ave., Cleveland, OH 44106-6009, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-56470

ACRONYM: HL

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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