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Journal of the American Society of Nephrology, Vol 5, 1120-1124, Copyright © 1994 by American Society of Nephrology

REGULAR ARTICLES

Renal vasoconstriction with U-46,619; role of arachidonate metabolites

CS Wilcox, WH Folger and WJ Welch
Department of Medicine, Pharmacology, and Therapeutics, University of Florida, College of Medicine, Gainesville.

Thromboxane A2 (TxA2) or its stable mimetic U-46,619 can increase the generation of arachidonate metabolites. Therefore, these studies were designed to investigate the role of prostaglandins, TxA2, and leukotrienes in the renal vascular response to U-46,619. Anesthetized rats were studied during a basal period and during an intra-aortic infusion of vehicle or U-46,619 (1 micrograms/kg per minute). U-46,619 reduced the GFR and the RBF without changing the mean arterial pressure or the femoral vascular resistance. All of the effects of U-46,619 were blocked by pretreatment with the TxA2/prostaglandin H2 receptor antagonist SQ-29,548. Pretreatment with the cyclo-oxygenase inhibitor indomethacin did not modify the renal vascular response to U-46,619. However, pretreatment with the TxA2 synthesis inhibitor UK-38,485 or with the leukotriene D4/E4 antagonist LY-163,443 markedly blunted the U- 46,619-induced increase in renal vascular resistance and the decrease in GFR. These results indicate that the renal vascular response to U- 46,619 is receptor mediated and is promoted by TxA2 and leukotriene D4/E4.


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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673