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The influence of changes in extracellular and intracellular sodium concentration on detrusor contractility
Author(s) -
BESARANI DLER,
WU CHANGHAO,
FRY CHRISTOPHER H.
Publication year - 2006
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2006.06061.x
Subject(s) - carbachol , chemistry , extracellular , isometric exercise , intracellular , contractility , contracture , biophysics , contraction (grammar) , medicine , muscle contraction , endocrinology , stimulation , biochemistry , biology , surgery
OBJECTIVE To determine the role of Na + ‐Ca 2+ exchange in the regulation of isolated detrusor smooth muscle contractility. MATERIALS AND METHODS Isolated guinea‐pig detrusor strips were used to record isometric tension generated by; (a) electrical‐field stimulation to elicit nerve‐mediated responses; and (b) adding carbachol or superfusing with a high‐K + solution. The [Na + ] gradient between extracellular and intracellular compartments was altered by: (i) reducing superfusate [Na + ] in stages from 140.2 to 10.2 m m ; (ii) addition of the cardiac glycoside strophanthidin (200 µ m ). RESULTS Reducing extracellular [Na + ] reversibly reduced the magnitude of nerve‐mediated contractions but increased the resting tension and magnitude of carbachol‐induced contracture. The mean ( sd ) [Na + ] required for a half‐maximum effect on attenuating contractions, at 85.9 (6.2) m m , and developing contracture, at 59.1 (14.3) m m , were significantly different. The time constants of changes to nerve‐mediated contractions and carbachol contracture were also significantly different, at 147 (5) vs 1207 (386) s, respectively. These differences suggest that separate mechanisms influence nerve‐mediated contraction and contracture in low‐Na + solutions. Exposure to the cardiac glycoside strophanthidin produced a similar effect to low‐Na + solutions for carbachol contracture. Low‐Na + solutions had no significant effect on contractures induced by high extracellular [K + ]. CONCLUSION Reducing the transmembrane [Na + ] difference increases intracellular [Ca 2+ ]. This increase is largely accommodated in intracellular stores, that can be released by exogenous carbachol. The results are consistent with the presence of a functional Na + ‐Ca 2+ exchanger in the surface membrane. The lack of effect of low‐Na + solutions on contractures evoked by membrane depolarization is consistent with this conclusion. The reduction of the nerve‐mediated contraction by low‐Na + solution might result from blockade of the nerve action potential.