Chronic hypoxia upregulates endothelial and inducible NO synthase gene and protein expression in rat lung

Timothy D. Le Cras, Chun Xue, Appavoo Rengasamy, Roger A. Johns

Research output: Contribution to journalArticlepeer-review

Abstract

The effect of chronic hypoxia-induced pulmonary hypertension on nitric oxide synthase (NOS) in the lung is controversial. To clarify the regulation of endothelial and inducible NOS (eNOS and iNOS) expression in the chronically hypoxic lung, Northern and Western blot analyses were performed on mRNA and total protein from lungs of rats exposed to 3 wk of hypoxia (10% O2, normobaric) or normoxia. Expression of the mRNA and protein for eNOS was significantly increased (1.6-fold and 2.1-fold, respectively) by hypoxia. Immunohistochemistry with an isoform-specific antibody demonstrated de novo expression of eNOS in the endothelium of resistance vessels in the pulmonary vasculature of the hypoxic rats. eNOS was detected in the endothelium of large vessels in both normoxic and hypoxic rat lungs. The level of mRNA and protein for iNOS was also found to be significantly increased (1.9-fold and 1.4-fold, respectively). In addition to the 4.4-kilobase (kb) iNOS mRNA species, a novel 4.0-kb species was also induced by hypoxia. We conclude that expression of eNOS and iNOS was increased in the lungs of rats subjected to chronic hypoxia, and that there was de novo expression of eNOS protein in the microvascular endothelium.

Original languageEnglish (US)
Pages (from-to)L164-L170
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume270
Issue number1 14-1
DOIs
StatePublished - Jan 1996
Externally publishedYes

Keywords

  • endothelial nitric oxide synthase
  • inducible nitric oxide synthase
  • nitric oxide
  • pulmonary hypertension

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

Fingerprint Dive into the research topics of 'Chronic hypoxia upregulates endothelial and inducible NO synthase gene and protein expression in rat lung'. Together they form a unique fingerprint.

Cite this