J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M300183-JLR200 on September 1, 2003

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Journal of Lipid Research, Vol. 44, 2391-2399, December 2003
Copyright © 2003 by American Society for Biochemistry and Molecular Biology

12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels

Shih Shen Yiu§, Xueying Zhao*,{dagger}, Edward W. Inscho{dagger} and John D. Imig1,*,{dagger}

* Vascular Biology Center, Medical College of Georgia, Augusta, GA 30912
{dagger} Department of Physiology, Medical College of Georgia, Augusta, GA 30912
§ Tulane University School of Medicine, New Orleans, LA 70112

1 To whom correspondence should be addressed. e-mail: jdimig{at}mail.mcg.edu

The lipoxygenase (LO) metabolite, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], constricts renal vessels, contributes to the vascular response to angiotensin, and has been implicated in cardiovascular and renal diseases. The current studies were performed to determine if renal microvascular 12(S)-HETE production is stimulated by angiotensin and the contribution of L-type calcium channels to the vasoconstriction elicited by 12(S)-HETE. Angiotensin increased renal microvascular 12(S)-HETE production by 64%, whereas cyclooxygenase metabolite production was not altered. Renal microvessels also expressed platelet-type 12-LO and leukocyte-type 12-LO. In the juxtamedullary preparation, afferent arteriolar diameter averaged 21 ± 1 µm and 12(S)-HETE caused a graded decrease in vessel caliber. The afferent arteriolar response to 12(S)-HETE was abolished during L-type calcium channel inhibition. Renal microvascular smooth muscle cells were studied using fluorescence microscopy. Renal myocyte [Ca2+]i averaged 93 ± 5 nmol/l. The 12(S)-HETE (5 µmol/l) increased myocyte [Ca2+]i to a peak value of 340 ± 55 nmol/l. The peak [Ca2+]i response following exposure to 12(S)-HETE was greatly attenuated in the absence of extracellular Ca2+ or calcium channel blockade.

These results demonstrate that renal microvascular 12(S)-HETE production is increased in response to angiotensin, and activation of L-type calcium channels is an important mechanism responsible for the afferent arteriolar vasoconstriction elicited by 12(S)-HETE.

Supplementary key words lipoxygenase • cytosolic calcium • microcirculation • kidney


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