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Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 59226
The present study
examined the effects of ANG II on the renal synthesis of
20-hydroxyeicosatetraenoic acid (20-HETE) and its contribution to the
renal vasoconstrictor and the acute and chronic pressor effects of ANG
II in rats. ANG II (10
11 to 107
mol/l) reduced the diameter of renal interlobular arteries treated with
inhibitors of nitric oxide synthase and cyclooxygenase, lipoxygenase, and epoxygenase by 81 ± 8%. Subsequent blockade of the synthesis of 20-HETE with 17-octadecynoic acid (1 µmol/l) increased the ED50 for ANG II-induced constriction by a factor of 15 and
diminished the maximal response by 61%. Graded intravenous infusion of
ANG II (5-200 ng/min) dose dependently increased mean arterial
pressure (MAP) in thiobutylbarbitol-anesthetized rats by 35 mmHg. Acute blockade of the formation of 20-HETE with dibromododecenyl
methylsulfimide (DDMS; 10 mg/kg) attenuated the pressor response to ANG
II by 40%. An intravenous infusion of ANG II (50 ng · kg1 · min1) in rats
for 5 days increased the formation of 20-HETE and epoxyeicosatrienoic acids (EETs) in renal cortical microsomes by 60 and 400%,
respectively, and increased MAP by 78 mmHg. Chronic blockade of the
synthesis of 20-HETE with intravenous infusion of DDMS (1 mg · kg1 · h1) or EETs and
20-HETE with 1-aminobenzotriazole (ABT; 2.2 mg · kg1 · h1) attenuated
the ANG II-induced rise in MAP by 40%. Control urinary excretion of
20-HETE averaged 350 ± 23 ng/day and increased to 1,020 ± 105 ng/day in rats infused with ANG II (50 ng · kg1 · min1) for 5 days. In contrast, urinary excretion of 20-HETE only rose to 400 ± 40 and 600 ± 25 ng/day in rats chronically treated with ANG II
and ABT or DDMS respectively. These results suggest that acute and
chronic elevations in circulating ANG II levels increase the formation
of 20-HETE in the kidney and peripheral vasculature and that 20-HETE
contributes to the acute and chronic pressor effects of ANG II.
cytochrome P-450; epoxyeicosatrienoic acids; hypertension; kidney
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