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Articles in PresS, published online ahead of print January 28, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00244.2001
Submitted on August 2, 2001
Accepted on January 11, 2002
1 Faculty of Medicine, Institute of Pharmacology & Therapeutics, Porto, Portugal
This study examined the effects of D2-like dopamine receptor activation upon Na+-K+-ATPase activity, while measuring apical-to-basal ouabain-sensitive amphotericin B-induced increases in short circuit current, and basolateral K+ (IK) currents in renal opossum kidney (OK) cells. The inhibitory effect of dopamine upon Na+-K+-ATPase activity was completely abolished by either D1- or D2-like receptor antagonists, and mimicked by D1- and D2-like receptor agonists, respectively SKF 38393 and quinerolane. Blockade of basolateral K+ channels with barium chloride (1 mM) or glibenclamide (10 µM), but not apamin (1 µM), totally prevented the inhibitory effects of quinerolane. The K+ channel opener pinacidil decreased Na+-K+-ATPase activity. The inhibitory effect of quinerolane upon Na+-K+-ATPase activity was abolished by pre-treatment of OK cells with pertussis toxin (PTX). Quinerolane increased, in a concentration dependent manner, IK across the basolateral membrane, this effect being abolished by pre-treatment with PTX, S-sulpiride and glibenclamide. SKF 38393 did not change IK. Both H-89 (PKA inhibitor) and chelerythrine (PKC inhibitor) failed to prevent the stimulatory effect of quinerolane upon IK. The stimulation of D2-like receptor was associated with a rapid hyperpolarizing effect, whereas D1-like receptor activation was accompanied by increases in cell membrane potential. It is concluded that stimulation of D2-like receptors leads to inhibition of Na+-K+-ATPase activity and hyperpolarization, both effects being associated with the opening of K+ channels.
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