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1 Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
2 Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Physiology, University of Maryland School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: tpallone{at}medicine.umaryland.edu.
Strong inward rectifier potassium channels are expressed by some vascular smooth muscle cells and facilitate K+ induced hyperpolarization. Using whole cell patch clamp of isolated descending vasa recta (DVR) we tested whether strong inward rectifier K+ currents (KIR) are present in smooth muscle / pericytes. Increasing extracellular K+ from 5 to 50 and 140 mmol/L induced inward rectifying currents. Those currents were Ba2+ sensitive and reversed at the K+ equilibrium potential (EK) imposed by the electrode and extracellular buffers. Ba2+ binding constants in symmetrical K+ varied between 0.24 and 24 µmol/L at -150 and -20 mV, respectively. Ba2+ blockade was time and voltage dependent. Extracellular Cs+ also blocked the inward currents with binding constants between 268 and 4938 µmol/L at -150 and -50 mV respectively. Ba2+ (30 µmol/L) and ouabain (1 mmol/L) depolarized pericytes by an average of 11 and 24 mV, respectively. Elevation of extracellular K+ from 5 to 10 mmol/L hyperpolarized pericytes by 6 mV. That hyperpolarization was reversed by Ba2+ (30 µmol/L). We conclude that strong inward rectifier K+ channels and Na+K+ATPase contribute to resting potential and that KIR channels can mediate K+ induced hyperpolarization of DVR pericytes.
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