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1Division of Nephrology, Department of Medicine, and 2Department of Physiology, University of Maryland School of Medicine, Baltimore; and 3Department of Biology, Towson University, Towson, Maryland
Submitted 21 March 2005 ; accepted in final form 22 July 2005
Using nystatin-perforated patch-clamp and whole cell recording, we tested the hypothesis that KATP channels contribute to resting conductance of rat descending vasa recta (DVR) pericytes and are modulated by vasoconstrictors. The KATP blocker glybenclamide (Glb; 10 µM) depolarized pericytes and inhibited outward currents of cells held at 40 mV. KATP openers pinacidil (Pnc; 10 µM) and P-1075 (1 µM) hyperpolarized pericytes and transiently augmented outward currents. All effects of Pnc and P-1075 were fully reversed by Glb. Inward currents of pericytes held at 60 mV in symmetrical 140 mM K+ were markedly augmented by Pnc and fully reversed by Glb. Ramp depolarizations in symmetrical K+, performed in Pnc and Pnc + Glb, yielded a Pnc-induced, Glb-sensitive KATP difference current that lacked rectification and reversed at 0 mV. Immunostaining identified both KIR6.1, KIR6.2 inward rectifier subunits and sulfonurea receptor subtype 2B. ANG II (1 and 10 nM) and endothelin-1 (10 nM) but not vasopressin (100 nM) significantly lowered holding current at 40 mV and abolished Pnc-stimulated outward currents. We conclude that DVR pericytes express KATP channels that make a significant contribution to basal K+ conductance and are inhibited by ANG II and endothelin-1.
kidney; medulla; microcirculation; electrophysiology; vasoconstriction
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