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Articles in PresS, published online ahead of print August 21, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0064.2001
Submitted on February 26, 2001
Accepted on August 14, 2001
1 Molecular Biomedicine, Centro de Investigacion y de Estudios Avanzados IPN, Mexico, D.F., Mexico
2 Pharmacology, New York Medical College, Valhalla, NY, USA
3 College of Pharmacy and Health Sciences, Texas Southern University, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: John_McGiff{at}NYMC.edu.
We examined the rat proximal tubule (PT) response to ET-1 in terms of 20-HETE dependency. Arachidonic acid (AA) (1 µM) decreased 86Rb uptake from 2.4±0.2 to 0.6±0.2 ng Rb/10 µg protein/2 min (p<0.05); 20-HETE (1 µM) had similar effects. DBDD (2 µM), an inhibitor of 
-hydroxylase, abolished the inhibitory action of AA on 86Rb uptake whereas the PT response to 20-HETE was unaffected. ET-1 at 0.1, 1, 10 and 100 nM reduced 86Rb uptake in PTs from 5.3±0.7 to 4.8±0.3, 4.0±0.6, 2.5±0.6 and 1.6±0.3 ng 86Rb/10 µg protein/2 minutes, respectively. DBDD (2 µM) abolished the inhibitory effect of ET-1 on 86Rb uptake as did BMS182874 (1 µM), an ETA-selective receptor antagonist. ET-1 (100 nM) significantly increased PT 20-HETE release by ca 50%, an effect prevented by DBDD. L-NAME, given for 4 days to inhibit nitric oxide synthase (NOS), increased arterial pressure from 92±12 to 140±8 mmHg and increased endogenous release of 20-HETE from isolated PTs (measured by GC/MS). In L-NAME-treated PTs, but not in control PTs, 0.1 µM AA inhibited 86Rb uptake by ~70%, which was attenuated by DBDD. We conclude that in the PTs, 1) 20-HETE is a second messenger for ET-1 and 2) 20-HETE-ET-1 interactions are augmented when NOS is inhibited.
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