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The change in the threshold for short‐term desensitization in isolated smooth muscle cells showing an all‐or‐none response to acetylcholine
Author(s) -
Mita Mitsuo,
Uchida Masaatsu K.
Publication year - 1991
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.1476-5381.1991.tb12476.x
Subject(s) - desensitization (medicine) , acetylcholine , contraction (grammar) , medicine , endocrinology , chemistry , collagenase , muscle contraction , biophysics , homologous desensitization , receptor , biology , biochemistry , enzyme
1 Isolated smooth muscle cells from guinea‐pig taenia caecum were prepared by collagenase digestion. The cells showed an all‐or‐none response to acetylcholine (ACh) under our experimental conditions. 2 Desensitized cells showed an all‐or‐none response but required a higher concentration of ACh for induction of contraction, indicating that the desensitization was due to a change in the threshold concentration. 3 In [ 3 H]‐quinuclidinyl benzilate ([ 3 H]‐QNB) binding to the desensitized cells, K D and B max were not significantly different from those estimated in the control cells. The competitive inhibition curve for specific binding of [ 3 H]‐QNB by ACh in the desensitized cells was in agreement with that of control cells. 4 The ACh‐stimulated increase of the 45 Ca 2+ influx was very rapid and correlated well with the contraction of the cells. The concentrations of ACh inducing the maximal 45 Ca 2+ influx were increased by desensitization. 5 These results indicated that although the binding of ACh to the receptor was not changed by desensitization, the threshold concentration of ACh for their contraction was raised by desensitization, and the 45 Ca 2+ influx accompanying the contraction was shifted to the side of high concentration of ACh. 6 These results suggest that the development of short‐term desensitization is due to an uncoupling of the receptor from the mechanism for initiation of the contraction.