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Cellular mechanism and computational modeling of the conductive arterial hyperpolarization/dilation
Author(s) -
Jiang ZhiGen,
Chen FangYi,
Ma KeTao
Publication year - 2010
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.24.1_supplement.974.6
Subject(s) - hyperpolarization (physics) , biophysics , membrane potential , resting potential , reversal potential , chemistry , intracellular , conductance , electrophysiology , patch clamp , physics , neuroscience , biology , stereochemistry , biochemistry , condensed matter physics , nuclear magnetic resonance spectroscopy
Evoked focal hyperpolarization and dilation (e.g., by ACh) can conduct along a small artery thus activate a fast blood flow surge; but the mechanism for such conduction remains unclear. Using intracellular and whole‐cell recording of guinea pig arterial cells and mathematical modeling, we found: (1) The resting potentials (RP) of sampled cells showed a bimodal distribution peaked near −75 and −40 mV. A cell initially having a low RP may swiftly shift to a high RP state and vice versa . Such shifts between the two RP levels were mimicked by wash‐in and ‐out of Ba 2+ (≤100 μM). Whole‐cell I/V showed an inward rectification that was sensitive to [K + ] o and Ba 2+ . (2) ACh induced a robust hyperpolarization or outward current at ~−40 mV, that was blocked by a 18β‐glycyrrhetinic acid plus Ba 2+ in smooth muscle cells. (3) Data of dual cell recording and cell labeling indicated a gap junction coupling among the vessel cells. (4) Whole‐cell I/V curves of dispersed cells could be math‐modeled by a sum of two voltage‐dependent (K ir , K DR ) and three voltage‐independent ion currents. (5) Inputting the five currents’ conductance means and their random variations into GHK zero‐current equation, and letting our custom‐written software seek individual RPs, we reproduced a bimodal RP distribution peaked near −75 and −40 mV. With timed alteration of ion conductances, the computation also simulated regenerative fast RP shift between the two RP levels. We conclude: 1) The arterial cells express abundant inward rectifier K + ‐channels (K ir ), which critically underlies the regenerative RP shift due to its unique voltage dependency. 2) Together with the gap junction coupling and Na‐K‐pump energy replenishing mechanism, the artery satisfies the minimal requisites for non‐decay conduction of the hyperpolarization/dilation. Supported by grant of NIH NIDCD DC004716.