Premium
Inward rectifier K + ‐channel and electrical coupling form the conduction mechanism of the EDHF‐induced arterial hyperpolarization
Author(s) -
Jiang ZhiGen,
Guan BingCai,
Yang YuQin
Publication year - 2006
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.20.4.a281-c
Subject(s) - hyperpolarization (physics) , biophysics , inward rectifier potassium ion channel , intracellular , membrane potential , resting potential , chemistry , anatomy , biology , ion channel , biochemistry , stereochemistry , receptor , nuclear magnetic resonance spectroscopy
Focal hyperpolarization and dilation induced by EDHF‐releasing agent (e.g., ACh) can conduct along the vessel but the cellular mechanism for such conduction remains unclear. Using intracellular or whole‐cell recording combining with cell labeling techniques on guinea pig in vitro spiral modiolar artery, we found: 1) The initial resting potentials (RP) in sampled cells showed a bimodal distribution peaked near −75 (high RP) and −40 mV (low RP). A cell initially having a low RP may swiftly shift to high RP state and vice versa . 2) Ba 2+ (1–100 μM) always caused a shift from high RP to low RP by its wash‐in and a reversed shift by its wash‐out. An overshot was often seen in the end of fast shift in both directions. Whole‐cell current showed an inward rectification that was sensitive to Ba 2+ . 3) ACh‐induced a robust hyperpolarization or outward current at ~−40 mV, that was blocked by a gap junction blocker 18β‐glycyrrhetinic acid plus Ba 2+ in smooth muscle (SMC), but not in endothelial cells (EC). 4) Data of dual cell recording, GRA effects on K + ‐induced hyperpolarization and cell labeling indicated a heterogeneous electrocoupling among cells and a macroscopic myoendothelial coupling efficiency of 0.49. We conclude that the vascular SMCs express abundant inward rectifier K + ‐channels (K ir ); the ACh‐induced hyperpolarization originates in the EC, electrotonically spreads to the muscular layer and in turn activates the K ir in the SMCs; the intercellular electrocoupling and the positive feed back by the loop of hyperpolarization→K ir disinhibition→further hyperpolarization in muscle cells form the cellular basis for the conductive inhibition. Supported by grant of NIH NIDCD DC004716.