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Articles in PresS, published online ahead of print June 30, 2002
J Appl Physiol, 10.1152/jap.00247.2002
Submitted on March 25, 2002
Accepted on June 21, 2002
1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA
3 Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: ejacobs{at}mcw.edu.
In contrast to its constrictor effects on peripheral arteries, 20-hydroxyeicosatetraenoic acid (20-HETE) is an endothelial dependent dilator of pulmonary arteries (PA). The present study examined the hypothesis that the vasodilator effects of 20-HETE in pulmonary arteries are due to an elevation of intracellular calcium concentration ([Ca2+]i) and the release of nitric oxide (NO) from bovine pulmonary artery endothelial cells (BPAECs). BPAECs express cytochrome P450 4A (CYP4A) protein and produce 20-HETE. 20-HETE dilated PAs preconstricted with U46619 or norepinephrine and treated with the cytochrome P450 inhibitor, 17-octadecynoic acid (17-ODYA) and the cyclooxygenase inhibitor, indomethacin. The dilator effect of 20-HETE was blocked by the nitric oxide synthase inhibitor, N
-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 NOS inhibitors (L-NAME). These results suggest that 20-HETE dilates pulmonary arteries at least in part by increasing [Ca2+]i and NO release in BPAECs.
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