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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: rroman{at}mcw.edu.
This study examined the effects of chronic blockade of the renal formation of epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE) with 1-aminobenzotriazole (ABT) (50 mg/kg/day, i.p. for 5 days) on pressure-natriuresis and the inhibitory effects of elevations in renal perfusion pressure (RPP) on Na+-K+-ATPase activity and the distribution of the sodium-hydrogen exchanger (NHE3) in the proximal tubule of rats. In control rats (N=15), sodium excretion rose from 2.3±0.4 to 19.4±1.8 µEq/min/g kwt when RPP was increased from 114±1 to 156±2 mmHg. Fractional excretion of lithium (FELi) rose from 28±3 to 43±3 % of the filtered load. Chronic treatment of the rats with ABT for 5 days (N=8) blunted the natriuretic response to elevations in RPP by 75% and attenuated the increase in FELi by 45%. In vehicle-treated rats, renal Na+-K+-ATPase activity fell from 31±5 to 19±2 µmol Pi/mg protein/hr and NHE3 protein was internalized from the brush border of the proximal tubule following an elevation in RPP. In contrast, Na+-K+-ATPase activity and the distribution of NHE3 protein remained unaltered in rats treated with ABT. These results suggest that cytochrome P450 metabolites of arachidonic acid contribute to pressure-natriuresis by inhibiting Na+-K+-ATPase activity and promoting internalization of NHE3 protein from the brush border of the proximal tubule.
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