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Expression of Inwardly Rectifying Potassium Channels in Descending Vasa Recta Endothelial Cells
Author(s) -
Cao Chunhua,
LeeKwon Whaseon,
Payne Kristie,
Pallone Thomas
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a956-d
Subject(s) - extracellular , biophysics , hyperpolarization (physics) , chemistry , patch clamp , gap junction , membrane potential , inward rectifier potassium ion channel , potassium channel , ouabain , biochemistry , ion channel , intracellular , biology , sodium , receptor , stereochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
Descending vasa recta (DVR) are 12–15‐μm vessels that supply blood flow to the renal medulla. The whole cell patch‐clamp method was used to investigate inward rectifier potassium channel (K IR ) activity in DVR endothelia. The endothelial monolayer was accessed by removing abluminal pericytes from collagenase digested vessels. K IR currents were recorded in symmetrical 140 mM external K + solution that served to both maximize K IR currents and eliminate prolonged capacitance transients by closing gap junctions. Large, Ba 2+ sensitive, inwardly rectifying currents were observed at membrane potentials less than the K + equilibrium potential. Ba 2+ potently inhibited K IR currents in a voltage dependent manner, with affinity, K d = 0.18, 0.33, 0.60, 1.20 μmol/L at −160, −120, −80 and −40mV, respectively. Extracellular Cs + also blocked the K IR currents with K d = 15, 33, 246 and 2266 μmol/L at −160, −120, −80 and −40mV, respectively. In the presence of 1 mM ouabain, elevation of extracellular K + from 5 to 10 mmol/L hyperpolarized membrane potential by 15 mV, which was reversed by Ba 2+ (30 μmol/L). Immunochemical staining verified that DVR expressK IR 2.1, K IR 2.2 and K IR 2.3 isoforms in both the pericytes and endothelium. We conclude that K IR are expressed in DVR endothelial cells and that extracellular K + can mediate hyperpolarization through their activity. This work was supported by American Heart Association Grant # 0625404U.