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Articles in PresS, published online ahead of print August 13, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00211.2002
Submitted on June 5, 2002
Accepted on July 31, 2002
1 Department of Pharmacology, New York Medical College, Valhalla, NY, USA
* To whom correspondence should be addressed. E-mail: wenhui_wang{at}nymc.edu.
We used the patch-clamp technique to study the effect of angiotensin II (AII) on the basolateral K channels in the cortical collecting duct (CCD). Application of AII (100 pM-100 nM) increased the activity of the basolateral 18 pS K channel. The effect of AII was completely abolished by losartan, an antagonist of AT1 receptor. In contrast, inhibition of AT2 receptor did not block the stimulatory effect of AII. Also, application of AII significantly increased intracellular Ca2+ measured with fura-2 dye. To explore the role of the Ca2+ -dependent pathways in the regulation of basolateral K channels, the effect of AII on channel activity was examined in the presence of arachidonyltrifluoromethyl ketone (AACOCF3) to inhibit phospholipase A2 (PLA2), GF109203x (PKC inhibitor) and L-NG-nitro-arginine methyl ester (L-NAME) to inhibit nitric oxide synthase (NOS), respectively. Inhibition of either PLA2 or PKC did not block the effect of AII on basolateral K channel activity. However, the stimulatory effect of AII was absent in the CCDs treated with L-NAME. Moreover, addition of the membrane-permeant 8-bromo-cGMP not only increased the channel activity but also abolished the stimulatory effect of AII on the channel activity. We conclude that AII increases the basolateral K channels via the stimulation of AT1 receptor and the stimulatory effect of AII is mediated by a NO-dependent cGMP pathway.
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