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1 Department of Pharmacology, New York Medical College, Valhalla, New York 10595; and 2 Department of Cell Biology, University of Medicine and Dentistry of New Jersey, Stratford, New Jersey 08084
The protean properties of
20-hydroxyeicosatetraenoic acid (HETE), vasoactivity, mitogenicity, and
modulation of transport in key nephron segments, serve as the basis for
the essential roles of 20-HETE in the regulation of the renal
circulation and electrolyte excretion and as a second messenger for
endothelin-1 and mediator of selective renal effects of ANG II. Renal
autoregulation and tubular glomerular feedback are mediated by 20-HETE
through constriction of preglomerular arterioles, responses that are
maintained by 20-HETE inhibition of calcium-activated potassium
channels. 20-HETE modulates ion transport in the proximal tubules and
the thick ascending limb by affecting the activities of
Na+-K+-ATPase
and the
Na+-K+-2Cl
cotransporter, respectively. The range and diversity of activity of
20-HETE derives in large measure from COX-dependent
transformation of 20-HETE to products affecting vasomotion and salt and
water excretion. Nitric oxide (NO) exerts a negative modulatory effect on 20-HETE formation; inhibition of NO synthesis produces marked perturbation of renal function resulting from increased 20-HETE production. 20-HETE is an essential component of interactions involving several hormonal systems that have central roles in blood
pressure homeostasis, including angiotensins, endothelins, NO, and
cytokines. 20-HETE is the preeminent renal eicosanoid, overshadowing
PGE2 and
PGI2. This review is
intended to provide evidence for the physiological roles for
cytochrome P-450-derived eicosanoids,
particularly 20-HETE, and seeks to extend this knowledge to a
conceptual framework for overall cardiovascular function.
20-hydroxyeicosatetraenoic acid; cyclooxygenase; cytochrome P-450 monooxygenases; endothelin; nitric oxide; potassium channels; preglomerular microvessels; renal autoregulation; thick ascending limb; tubuloglomerular feedback; tumor necrosis factor
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