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Modulation of the isoprenaline‐induced membrane hyperpolarization of mouse skeletal muscle cells
Author(s) -
Mil H.G.J.,
Kerkhof C.J.M.,
Heukelom J. Siegenbeek
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15940.x
Subject(s) - hyperpolarization (physics) , membrane potential , depolarization , ouabain , chemistry , isoprenaline , forskolin , biophysics , medicine , sodium , biochemistry , stereochemistry , biology , stimulation , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1 The hyperpolarization of the resting membrane potential, V m , induced by isoprenaline in the lumbrical muscle fibres of the mouse, was investigated by use of intracellular microelectrodes. 2 In normal Krebs‐Henseleit solution (potassium concentration: K + o =5.7mM, ‘control’), V m was −74.0 ± 0.2 mV; lowering K + o to 0.76 mM (′low K + o ) resulted in either a hyperpolarization (V m = −95.7 ±2.9 mV), or a depolarization (V m = −52.0 ±0.3 mV). 3 Isoprenaline (≥200 nM) induced a hyperpolarization of V m by ΔV m = − 5.6 ±0.4 mV in control solution. 4 When V m hyperpolarized after switching to low K + o , the addition of isoprenaline resulted in increased hyperpolarization V m : ΔV m =−16.3±3.2 mV to a final V m =−110.1 ±3.4 mV. Adding iso‐prenaline when V m depolarized in low K + o , leads to a hyperpolarization of either by − 11.6±0.5mV to −63.6 ±0.8 mV or by −51.7 ±2.7 mV to −106.9 ±3.9 mV. 5 Ouabain (0.1 to 1 m m ) did not suppress the hyperpolarization by isoprenaline in 5.7 mM K + o (ΔV m =−6.7±0.4mV) or the hyperpolarization of the depolarized cells in low K+ o (ΔV m =−9.7 Δ1.5mV). 6 The hyperpolarization is a logarithmically decreasing function of K + o in the range between 2 and 20 mM (12 mV/decade). 7 IBMX and 8Br‐cyclic AMP mimicked the response to isoprenaline whereas forskolin (FSK) induced in low K + o a hyperpolarization of −7.0 ±0.7 mV that could be augmented by addition of isoprenaline (ΔV m =−8.2±1.8mV). 8 In control and low K + o , Ba 2+ (0.6 m m ) inhibited the hyperpolarization induced by isoprenaline, IBMX or 8Br‐cyclic AMP. Other blockers of the potassium conductance such as TEA (5 m m ) and apamin (0.4 μ m ) had no effect. 9 We conclude that in the lumbrical muscle of the mouse the isoprenaline‐induced hyperpolarization is primarily due to an increase in potassium permeability.