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Endothelial K ir channels: Do they act as amplifiers of endothelial cell hyperpolarization?
Author(s) -
Marrelli Sean P
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.a1387-d
Subject(s) - hyperpolarization (physics) , vasodilation , inward rectifier potassium ion channel , potassium channel , patch clamp , agonist , chemistry , membrane potential , biophysics , medicine , ion channel , microbiology and biotechnology , endocrinology , biology , biochemistry , receptor , stereochemistry , nuclear magnetic resonance spectroscopy
Objective: We examined whether middle cerebral artery (MCA) endothelial cells express K ir channels, and if so, whether K ir channels act to amplify agonist‐stimulated endothelial cell (EC) hyperpolarization. EC hyperpolarization has been shown to directly promote vasodilatation. Methods: K ir 2.x channel RNA was evaluated in freshly isolated EC by RT‐PCR. K ir channel function was measured in EC by whole cell patch clamp. The role of K ir channels in EC hyperpolarization (voltage‐sensitive dye; di‐8‐ANEPPS) and vasodilatation was evaluated in intact pressurized MCA. Results: Freshly isolated EC expressed RNA for K ir 2.1 and 2.2, whereas whole MCA expressed K ir 2.1, 2.2, 2.3, and 2.4. Whole cell patch clamp in EC demonstrated a Ba 2+ ‐sensitive inwardly rectifying current. This current exhibited established characteristics of K ir channel currents. Luminal BaCl 2 (75 μM) was used to evaluate the functional role of K ir channels in agonist‐mediated (10 μM UTP) EC hyperpolarization and vasodilatation in pressurized MCA. Hyperpolarization and dilation to luminal UTP were both slightly reduced in the presence of BaCl 2 . Conclusion: We demonstrated that MCA EC express functional K ir channels that are likely of the K ir 2.1 or 2.2 subtype. These K ir channels contribute to UTP‐mediated vasodilatation and may act through amplification of EC hyperpolarization. Supported by AHA 0665100Y and 0230353N.