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1 Department of Medicine, University of Maryland, Baltimore, MD, USA; Department of Physiology, University of Maryland, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: tpallone{at}medicine.umaryland.edu.
We tested whether K+ channel inhibition accompanies angiotensin II (AngII) induced depolarization of descending vasa recta (DVR) pericytes. An increase in extracellular [K+] ([K+]o) from 5 to 100 mM depolarized resting pericytes but had no effect after prolonged (10 nM, 20 min) AngII exposure. In contrast, reduction of extracellular [Cl-] ([Cl-]o) from 154 to 34 mM had a minor effect on resting membrane potential but strongly depolarized pericytes treated with AngII. The K+ channel blockers, BaCl2 (0.1, 1 mM) and tetraethylammonium (TEA, 30 mM) depolarized resting pericytes but did not affect membrane potential of AngII treated pericytes. Pericyte whole cell currents were reduced by AngII and nearly eliminated by combined AngII exposure and the Cl- channel blocker, niflumic acid (100 µM). Augmentation of inward current induced by raising [K+]o from 5 to 50 mM was eliminated by pre-exposure to AngII. TEA and BaCl2 sensitive outward currents, generated by depolarizing pericytes from -80 to -40 mV, were eliminated by AngII. We conclude that AngII depolarizes DVR pericytes by a combination of Cl- channel activation and K+ channel inhibition.
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