KATPchannel conductance of descending vasa recta pericytes
Autor: | Thomas L. Pallone, Whaseon Lee-Kwon, Erik P. Silldorff, Chunhua Cao |
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Rok vydání: | 2005 |
Předmět: |
Vasopressins
Physiology Descending vasa recta Electric Capacitance Membrane Potentials Microcirculation Rats Sprague-Dawley KATP Channels Katp channels Glyburide medicine Animals Potassium Channels Inwardly Rectifying Endothelin-1 Chemistry Angiotensin II Pinacidil Conductance Vasa recta Anatomy Juxtaglomerular Apparatus Rats Cell biology Electrophysiology medicine.anatomical_structure ATP-Binding Cassette Transporters medicine.symptom Pericytes Whole cell Vasoconstriction |
Zdroj: | American Journal of Physiology-Renal Physiology. 289:F1235-F1245 |
ISSN: | 1522-1466 1931-857X |
DOI: | 10.1152/ajprenal.00111.2005 |
Popis: | Using nystatin-perforated patch-clamp and whole cell recording, we tested the hypothesis that KATPchannels contribute to resting conductance of rat descending vasa recta (DVR) pericytes and are modulated by vasoconstrictors. The KATPblocker glybenclamide (Glb; 10 μM) depolarized pericytes and inhibited outward currents of cells held at −40 mV. KATPopeners 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 KATPdifference 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 KATPchannels that make a significant contribution to basal K+conductance and are inhibited by ANG II and endothelin-1. |
Databáze: | OpenAIRE |
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