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Physiological Reviews, Vol. 82, No. 1, January 2002, pp. 131-185; 10.1152/physrev.00021.2001.
Copyright ©2002 by the American Physiological Society
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin
Roman, Richard J.
P-450 Metabolites of Arachidonic Acid in the
Control of Cardiovascular Function. Physiol. Rev. 82: 131-185, 2002.
Recent studies have
indicated that arachidonic acid is primarily metabolized by cytochrome
P-450 (CYP) enzymes in the brain, lung, kidney, and
peripheral vasculature to 20-hydroxyeicosatetraenoic acid (20-HETE) and
epoxyeicosatrienoic acids (EETs) and that these compounds play critical
roles in the regulation of renal, pulmonary, and cardiac function and
vascular tone. EETs are endothelium-derived vasodilators that
hyperpolarize vascular smooth muscle (VSM) cells by activating
K+ channels. 20-HETE is a vasoconstrictor produced in VSM
cells that reduces the open-state probability of
Ca2+-activated K+ channels. Inhibitors of the
formation of 20-HETE block the myogenic response of renal, cerebral,
and skeletal muscle arterioles in vitro and autoregulation of renal and
cerebral blood flow in vivo. They also block
tubuloglomerular feedback responses in vivo and the vasoconstrictor
response to elevations in tissue PO2 both in
vivo and in vitro. The formation of 20-HETE in VSM is stimulated by
angiotensin II and endothelin and is inhibited by nitric oxide (NO) and
carbon monoxide (CO). Blockade of the formation of 20-HETE attenuates
the vascular responses to angiotensin II, endothelin, norepinephrine,
NO, and CO. In the kidney, EETs and 20-HETE are produced in the
proximal tubule and the thick ascending loop of Henle. They regulate
Na+ transport in these nephron segments. 20-HETE also
contributes to the mitogenic effects of a variety of growth factors in
VSM, renal epithelial, and mesangial cells. The production of EETs and
20-HETE is altered in experimental and genetic models of hypertension, diabetes, uremia, toxemia of pregnancy, and hepatorenal syndrome. Given
the importance of this pathway in the control of cardiovascular function, it is likely that CYP metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with some of these conditions and that drugs that modify the
formation and/or actions of EETs and 20-HETE may have therapeutic benefits.
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