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Am J Physiol Heart Circ Physiol (July 8, 2002). doi:10.1152/ajpheart.00321.2002
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Articles in PresS, published online ahead of print July 8, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00321.2002
Submitted on April 10, 2002
Accepted on June 26, 2002

Evidence for a Membrane Site of Action for 14,15-EET on Expression of Aromatase in Vascular Smooth Muscle

Gary D. Snyder1*, U Murali Krishna2, J R. Falck2, and Arthur A. Spector1

1 Biochemistry, University of Iowa, Iowa City, IA, USA
2 Biochemistry, University of Texas Southwestern Medical School, Dallas, TX, USA

* To whom correspondence should be addressed. E-mail: gary-snyder{at}uiowa.edu.

Epoxyeicosatrienoic acids (EETs) are synthesized in the endothelial cells of vascular tissues. They are released from the endothelial cells and produce relaxation of the smooth muscle cells by hyperpolarization. The present findings demonstrate that EETs also regulate aromatase activity in vascular smooth muscle cells. Exposure of rat aortic smooth muscle cells to either 1 µM 14,15-EET or 1 µM 11,12-EET inhibits dibutyryl cyclic AMP-induced aromatase activity by 80% to 100%. In contrast to 14,15-EET, the N-methylsulfanilamide derivative of 14,15-EET (14,15-EET-SA) was neither metabolized nor incorporated into cell lipids, but it retained the ability to inhibit cyclic AMP-induced aromatase activity. Furthermore, the 14,15-EET-SA inhibition of cyclic AMP-stimulated aromatase activity persisted when the 14,15-EET-SA was covalently tethered to silica beads (average diameter, 0.5 µ) that restricted the 14,15-EET-SA from entering the cell. These data are consistent with the presence of a receptor for EETs in the plasma membrane and support the hypothesis that the inhibition of aromatase by EETs is initiated by the interaction of the EET with the putative membrane receptor.




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