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Vasodilatation and smooth muscle membrane potential changes in arterioles from the guinea‐pig small intestine.
Author(s) -
Kotecha N,
Neild T O
Publication year - 1995
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 - 10.1113/jphysiol.1995.sp020548
Subject(s) - vasoactive intestinal peptide , hyperpolarization (physics) , galanin , acetylcholine , medicine , vasodilation , endocrinology , arteriole , hexamethonium , chemistry , cholinergic , biology , neuropeptide , microcirculation , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. Dilatation of arterioles isolated from the guinea‐pig small intestine was evoked by stimulation of a submucous ganglion and the application of acetylcholine, vasoactive intestinal peptide, galanin or dynorphin A. Changes in arteriole diameter and smooth muscle membrane potential were recorded simultaneously. 2. Ganglion stimulation caused vasodilatation and smooth muscle hyperpolarization that varied in both amplitude and time course from one arteriole to another. Vasodilatation could occur without hyperpolarization. 3. Vasodilatation caused by acetylcholine was accompanied by a rapidly developing hyperpolarization that began to decline before the maximum vasodilator effect had developed. 4. Vasoactive intestinal peptide caused dilatation without any change in smooth muscle membrane potential. 5. Galanin and dynorphin caused dilatation and a hyperpolarization of similar time course to the dilatation. 6. In 48% of arterioles tested the dilatation appeared to be mediated solely by acetylcholine. In 31% there was a cholinergic component, but no evidence for the involvement of acetylcholine in the remaining 21%. When the non‐cholinergic dilatation occurred without a hyperpolarization we conclude that it was due to vasoactive intestinal peptide; otherwise it may have been due to either galanin or dynorphin.