Acute hypoxia increases intracellular L-arginine content in cultured porcine pulmonary artery enclothelial cells

Yunchao Su, Edward R. Block

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Exposure to hypoxia (0% O2) for 4-24 h resulted in increased intracellular L-arginine content and increased activity of calpain, a calcium-dependent neutral cysteine protease, in pulmonary artery endothelial cells. Calpain-inhibitor I abolished the increased L-arginine content in hypoxic cells. When endothelial cell proteins were labeled with [3H]-L-arginine and the cells exposed to hypoxia, we observed an increase in free [3H]-L-arginine and a decrease in [3H]-L-arginine-labeled proteins. Once again, calpain-inhibitor I prevented the increases in free [3H]-L-arginine and the decreases in [3H]-L-arginine-labeled proteins in hypoxic cells. Hypoxia also inhibited the synthesis of L-arginine-containing proteins. Thus, the increase in intracellular L-arginine content in hypoxic pulmonary artery endothelial cells is caused by an increase in proteolysis secondary to calpain and a decrease in protein synthesis. These results indicate that hypoxia can modulate the availability of free intracellular L-arginine, the exclusive precursor of nitric oxide (NO) and the primary substrate of NO synthase, by affecting the synthesis and degradation of cellular proteins.

Original languageEnglish (US)
Pages (from-to)349-353
Number of pages5
JournalJournal of Cellular Physiology
Volume167
Issue number2
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

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Pulmonary Artery
Arginine
Swine
Calpain
Endothelial cells
Proteins
Endothelial Cells
Proteolysis
Cells
Hypoxia
Cysteine Proteases
Nitric Oxide Synthase
Nitric Oxide
Availability
Calcium
Degradation
Substrates

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Acute hypoxia increases intracellular L-arginine content in cultured porcine pulmonary artery enclothelial cells. / Su, Yunchao; Block, Edward R.

In: Journal of Cellular Physiology, Vol. 167, No. 2, 01.01.1996, p. 349-353.

Research output: Contribution to journalArticle

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