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1 Division of Nephrology, Department of Medicine, University of Maryland Schoool of Medicine, Baltimore, MD, USA
2 Department of Biology, Towson University, Towson, MD, USA
3 Division of Nephrology, Department of Medicine, University of Maryland Schoool of Medicine, Baltimore, MD, USA; Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: tpallone{at}medicine.umaryland.edu.
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. Angiotensin II (1 nM, 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 significant contribution to basal K+ conductance and are inhibited by AngII and ET-1.
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