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K + Channels Which Contribute to the Acetylcholine‐Induced Hyperpolarization in Smooth Muscle of the Guinea‐Pig Submucosal Arteriole
Author(s) -
Hashitani H.,
Suzuki H.
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.319bn.x
Subject(s) - hyperpolarization (physics) , depolarization , membrane potential , chemistry , acetylcholine , biophysics , resting potential , arteriole , reversal potential , electrophysiology , medicine , patch clamp , biochemistry , stereochemistry , biology , microcirculation , receptor , nuclear magnetic resonance spectroscopy
1 Membrane potentials were recorded from submucosal arterioles (diameter, 30–80 μm) of the guinea‐pig small intestine, using conventional microelectrode techniques. In control solution the resting membrane potential was about −73 mV, and the addition of 0.5 m m Ba 2+ depolarized the membrane to about −43 mV. 2 ACh (10 nm to 10 μM), or substance P (0.1 μM), caused a membrane hyperpolarization in preparations which had been depolarized by Ba 2+ but not in control preparations. ACh produced a sustained hyperpolarization, whereas substance P produced a transient hyperpolarization, without being affected by either nitroarginine (0.1 m m ) or indomethacin (10 μM). 3 In the presence of 50 μM BAPTA (acetoxymethyl ester form), the membrane potentials were not altered in the control solution or in the presence of Ba 2+ , but Ba 2+ caused a smooth depolarization of the membrane. Following this procedure, both ACh and substance P caused membrane depolarization instead of hyperpolarization, suggesting that the ACh‐ and substance P‐induced hyperpolarization in arteriolar smooth muscle are intracellular [Ca 2+ ] dependent. 4 In short segments (200–500 μM) of arteriole, the time constant of electrotonic potentials produced by passing current pulses through the recording electrode was about 75 ms. The addition of Ba 2+ increased both the input resistance and the time constant. 5 The hyperpolarizations produced by ACh or substance P were associated with a reduction in the amplitude and the time constant of electrotonic potential. 6 The reversal potential for the ACh‐induced hyperpolarization, estimated from the current‐voltage relationship, was about −86 mV, a value close to the equilibrium potential for K + . 7 In the presence of 50 nM charybdotoxin the hyperpolarization produced by ACh became transient and was reduced in amplitude: the residual response was further reduced by apamin (0.1 μM). The response produced by substance P was also reduced by 50 nM charybdotoxin: again the residual response was sensitive to 0.1 μM apamin. The hyper‐polarizations produced by either ACh or substance P were insensitive to glibenclamide (10 μM) and 4‐aminopyridine (1 m m ). 8 It is suggested that in submucosal arterioles of the guinea‐pig ileum, ACh‐ or substance P‐induced hyperpolarizations of smooth muscle result from activation of both charybdotoxin‐sensitive and apamin‐sensitive K + channels, with the former being predominant. The results are discussed in relation to the possible involvement of one or more endothelium‐dependent hyperpolarizing factors in ACh‐ and substance P‐induced hyperpolarization.