Premium
Kinetics of contraction in depolarized smooth muscle from guinea‐pig taenia coli after photodestruction of nifedipine
Author(s) -
Malmqvist Ulf,
Arner Anders
Publication year - 1999
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 - 10.1111/j.1469-7793.1999.0213o.x
Subject(s) - nifedipine , taenia coli , chemistry , biophysics , contraction (grammar) , depolarization , kinetics , extracellular , muscle contraction , calcium , anatomy , biochemistry , endocrinology , biology , physics , organic chemistry , quantum mechanics
1 The time course and kinetics of force development following activation by opening of L‐type Ca 2+ channels was investigated using photodestruction of the Ca 2+ channel blocker nifedipine in smooth muscle from the guinea‐pig taenia coli. 2 In muscles activated using high K + and Ca 2+ and subsequently inhibited with nifedipine, photodestruction of the drug using a strong ultraviolet light flash initiated a rapid contraction. The force initiated by photodestruction of nifedipine reached near‐maximal levels. This procedure eliminates diffusional delays and can thus be used to investigate the kinetics of depolarization‐induced contractions. 3 The rate of force development of contractions initiated by photodestruction of nifedipine was slower than that observed in maximally thiophosphorylated skinned fibres. This suggests the rate of force development is limited by activation steps in the activation cascade prior to the force generation of the cross‐bridge system. 4 The rate of force development and the plateau force were dependent on the extracellular [CaCl 2 ] suggesting that the intracellular [Ca 2+ ] determines the rate of phosphorylation and force development. The delay between illumination and increase in force was about 300 ms. The delay was similar at low and high extracellular [CaCl 2 ] indicating that buffering by superficial sarcoplasmatic reticulum does not introduce a delay in force development following activation of Ca 2+ channels in this muscle.