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S Ryang

Publications and source records attributed to S Ryang.

11 recordsLinked to original sources
PubMed1995

Characterization of muscarinic receptors mediating relaxation and contraction in the rat iris dilator muscle.

1. The characteristics of muscarinic receptors mediating relaxation and/or contraction in the rat iris dilator muscle were examined. 2. Relaxation was induced in a dilator muscle by application of acetylcholine (ACh) at low doses (3 microM or less) and contraction was induced by high doses. Methacholine and carbachol also showed biphasic effects similar to those of ACh; in contrast, bethanechol, arecoline, pilocarpine and McN-A-343 induced mainly relaxation but no substantial contraction. 3. After parasympathetic denervation by ciliary ganglionectomy, the relaxant response to muscarinic agonists disappeared upon nerve stimulation. Application of McN-A-343 and pilocarpine induced only small contractions in denervated dilator muscles, indicating that these are partial agonists for contraction. 4. pA2 values of pirenzepine, methoctramine, AF-DX 116, himbacine, and 4-DAMP for antagonism to pilocarpine-induced relaxation in normal dilator muscles and those for antagonism to ACh-induced contraction in denervated dilator muscles were determined. The pA2 values for antagonism to relaxation of all these antagonists were most similar to those for M3-type muscarinic receptors. 5. Although pA2 values for contraction of these antagonists, except for methoctramine, were very close to those for relaxation, contraction was not significantly antagonized by methoctramine. Contraction might be mediated by M3-like receptors which have a very low affinity for methoctramine. 6. In conclusion, ACh-induced biphasic responses in rat iris dilator muscles were clearly distinguished from each other by specific muscarinic agonists and parasympathetic denervation, whereas muscarinic receptors could not be subclassified according to the pA2 values of 5 specific antagonists only.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1990

Atropine-resistant relaxation induced by high K+ in iris dilator muscle of the rat and pig.

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 microM phentolamine, 1 microM propranolol and 1 or 10 microM atropine. High K+ (greater than 20 mM) induced a biphasic response; an initial phasic contraction followed by relaxation rather than tonic contraction. 2. An additional application of a Ca2+ antagonist, 1 microM 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 mM. 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 microM ouabain. The relaxation induced by 40 or 80 mM K+ in the porcine dilator was slightly enhanced or not affected, respectively, in the presence of 1 microM ouabain. Application of 10 microM 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 microM tetrodotoxin, 10 microM indomethacin, 10 JM 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 mM) or nitroprusside (1-100 microM). 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.

Animals↗