Inhibition of K+ conductance in descending vasa recta pericytes by ANG II.
We tested whether K(+) channel inhibition accompanies ANG II-induced depolarization of descending vasa recta (DVR) pericytes. An increase in extracellular K(+) concentration ([K(+)](o)) from 5 to 100 mM depolarized resting pericytes but had no effect after prolonged (10 nM, 20 min) ANG II exposure. In contrast, reduction of extracellular Cl(-) concentration ([Cl(-)](o)) from 154 to 34 mM had a minor effect on resting membrane potential but strongly depolarized pericytes treated with ANG II. The K(+) channel blockers BaCl(2) (0.1, 1 mM) and tetraethylammonium (TEA; 30 mM) depolarized resting pericytes but did not affect membrane potential of ANG II-treated pericytes. Pericyte whole cell currents were reduced by ANG II and nearly eliminated by combined ANG II exposure and the Cl(-) channel blocker niflumic acid (100 muM). Augmentation of inward current induced by raising [K(+)](O) from 5 to 50 mM was eliminated by preexposure to ANG II. TEA- and BaCl(2)-sensitive outward currents, generated by depolarizing pericytes from -80 to -40 mV, were eliminated by ANG II. We conclude that ANG II depolarizes DVR pericytes by a combination of Cl(-) channel activation and K(+) channel inhibition.
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201-1595, USA. tpallone@medicine.umaryland.edu
Thomas L
TL
Pallone
Chunhua
C
Cao
Zhong
Z
Zhang
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D018118:Chloride Channels / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000502:physiology; D002712:Chlorides / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology; D004553:Electric Conductivity; D007679:Kidney Medulla / Q000098:blood supply*; D008564:Membrane Potentials / Q000187:drug effects; D009544:Niflumic Acid / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D020286:Pericytes / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019789:Tetraethylammonium / Q000494:pharmacology
D017609:Barium Compounds; D018118:Chloride Channels; D002712:Chlorides; D026902:Potassium Channel Blockers; D015221:Potassium Channels; C024986:barium chloride; D000804:Angiotensin II; D009544:Niflumic Acid; D019789:Tetraethylammonium; D011188:Potassium