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RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Vasa recta pericytes express a strong inward rectifier K⁺ conductance

¹Division of Nephrology, Department of Medicine, and ²Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland

Submitted 14 December 2005 ; accepted in final form 23 January 2006

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 are present in smooth muscle and 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 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 4,938 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 K_IR channels can mediate K⁺-induced hyperpolarization of DVR pericytes.

kidney; medulla; microcirculation; electrophysiology; potassium channel

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