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Atropine‐resistant relaxation induced by high K + in iris dilator muscle of the rat and pig
Author(s) -
Ryang S.,
Takei S.,
Kawai T.,
Imaizumi Y.,
Watanabe M.
Publication year - 1990
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.1476-5381.1990.tb15818.x
Subject(s) - ouabain , dilator , atropine , chemistry , contraction (grammar) , phentolamine , propranolol , acetylcholine , muscle contraction , endocrinology , medicine , biophysics , sodium , biology , organic chemistry
1 The effects of high K + ion concentration on the isometric tension in dilator muscle strips of the rat and porcine iris were examined. A high K + solution, prepared by the replacement of Na + in the medium with equimolar K + , was applied in the presence of 1 μ m phentolamine, 1 μ m propranolol and 1 or 10 μ m atropine. High K + (> 20 m m ) induced a biphasic response; an initial phasic contraction followed by relaxation rather than tonic contraction. 2 An additional application of a Ca 2+ antagonist, 1 μ m nifedipine or nicardipine, almost completely blocked the K + ‐induced initial contraction and enhanced the following relaxation. The effect of K + under these conditions was concentration‐dependent in the range 20 to 80 m m . The maximum amplitude of the atropine‐resistant relaxation induced by high K + corresponds to 50–75% of that produced by acetylcholine in the absence of atropine. A similar K + ‐induced relaxation was observed in the porcine iris dilator. 3 The atropine‐resistant relaxation in the rat iris dilator was not affected by pretreatment with 10 μ m ouabain. The relaxation induced by 40 or 80 m m K + in the porcine dilator was slightly enhanced or not affected, respectively, in the presence of 1 μ m ouabain. Application of 10 μ m ouabain per se induced relaxation in the porcine iris dilator. 4 The low Na + ion concentration present in high K + solutions was not responsible for the K + ‐induced relaxation since the complete replacement of Na in the medium with Tris did not affect significantly the relaxation produced by high K + ‐containing solutions. 5 Neither 1 μ m tetrodotoxin, 10 μ m indomethacin, 10 μ m nordihydroguaiaretic acid nor hypoxic conditions affected the high K + ‐induced relaxation. 6 The inherent tone of the rat iris dilator was not affected by either 8‐bromo cyclic GMP, dibutyryl cyclic GMP (0.1‐0.3 m m ) or nitroprusside (1–100 μ m ). 7 These results may suggest that the atropine‐resistant relaxation induced by high K + is not due to either activation of the Na‐K pump or release of a relaxing factor produced by oxidative metabolism. Although the relaxation mechanism has not been elucidated, it is probably not mediated by an increase in cellular cyclic GMP levels.