| Autor: |
Chunhua Cao, Whaseon Lee-Kwon, Silldorff, Erik P., Pallone, Thomas L. |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Renal Physiology; Dec2005, Vol. 289, pF1235-F1245, 11p, 8 Color Photographs, 1 Chart, 36 Graphs |
| Abstrakt: |
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. 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 DYR pericytes express KATP channels that make a significant contribution to basal K+ conductance and are inhibited by ANG II and endothelin-1. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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