Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 93, Issue 4, Pages 1391-1399Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00247.2002
Keywords
cytochrome P-450; calcium transients; pulmonary artery endothelial cells; vasodilation; 20-hydroxyeicosatetraenoic acid
Categories
Funding
- NHLBI NIH HHS [HL-32887, P01 HL-59996, R37 HL036279, HL-49294] Funding Source: Medline
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In contrast to its constrictor effects on peripheral arteries, 20-hydroxyeicosatetraenoic acid (20-HETE) is an endothelial-dependent dilator of pulmonary arteries (PAs). The present study examined the hypothesis that the vasodilator effects of 20-HETE in PAs are due to an elevation of intracellular calcium concentration ([Ca2+](i)) and the release of nitric oxide (NO) from bovine PA endothelial cells (BPAECs). BPAECs express cytochrome P-450 4A (CYP4A) protein and produce 20-HETE. 20-HETE dilated PAs preconstricted with U-46619 or norepinephrine and treated with the cytochrome P-450 inhibitor 17-octadecynoic acid and the cyclooxygenase inhibitor indomethacin. The dilator effect of 20-HETE was blocked by the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) or by removal of endothelium. 20-HETE significantly increased [Ca2+](i) and NO production in BPAECs. 20-HETE-induced NO release was blunted by removal of extracellular calcium, as well as NO synthase inhibitors (L-NAME). These results suggest that 20-HETE dilates PAs at least in part by increasing [Ca2+](i) and NO release in BPAECs.
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