RT Journal Article SR Electronic T1 Inhibition of Na-K-Cl cotransport by amiloride analogues is associated with stimulation of cyclic AMP-dependent protein kinase. JF Molecular Pharmacology JO Mol Pharmacol FD American Society for Pharmacology and Experimental Therapeutics SP 393 OP 398 VO 44 IS 2 A1 R D Feldman A1 S J Dixon YR 1993 UL http://molpharm.aspetjournals.org/content/44/2/393.abstract AB Analogues of amiloride are widely used as pharmacological probes for inhibition of sodium-hydrogen counter-transport. In Jurkat cells, a leukemic T lymphocyte cell line, analogues of amiloride are also potent inhibitors of Na-K-Cl cotransport. The effects of these agents are not additive with those of beta-adrenoceptor agonists (which inhibit Na-K-Cl cotransport presumably by stimulation of adenylyl cyclase). Further, analogues of amiloride potently stimulate cAMP-dependent protein kinase activity. The present studies indicate that beta-adrenoceptor agonists and analogues of amiloride both act to inhibit Na-K-Cl cotransport and both stimulate cAMP-dependent protein kinase activity. Furthermore, these studies demonstrate a novel mechanism by which amiloride analogues may mediate effects separately from inhibition of sodium-hydrogen exchange.