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Differential roles for potassium and acetylcholine in producing the dilations resulting from a single tetanic skeletal muscle contraction
Author(s) -
Mihok Marika L,
Murrant Coral L
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a271-a
Subject(s) - contraction (grammar) , acetylcholine , potassium , muscle contraction , skeletal muscle , chemistry , biophysics , medicine , biology , organic chemistry
The rapid onset of the dilation within 2 seconds of a single tetanic contraction suggests that the dilators involved may be products of muscle activation (e.g. acetylcholine (ACh) and potassium (K + )). To investigate the role of ACh and K + in these rapid dilations we stimulated 4–5 skeletal muscle fibres in the anaesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at the site of overlap with the stimulated muscle fibres before and after a single contraction (250ms train duration) over a range of stimulus frequencies (4, 10, 20, 30, 40 and 60Hz). Muscle fibres were stimulated in the absence and presence of a muscarinic antagonist atropine (10 −5 M), Na + K + ATPase inhibitor ouabain (10 −4 M), K IR channel inhibitor barium chloride (5x10 −5 M), or Kv channel inhibitor 3,4‐diaminopyridine (10 −3 M). We observed significant inhibitions of the rapid dilation at all stimulus frequencies with inhibitors of Na + K + ATPase, K IR and Kv channels; across all stimulus frequencies, we observed an average decrease in dilation of 40.5+/−3.9%, 49.8+/−4.4% and 43.0+/−4.7% respectively. Atropine did not inhibit the rapid dilation (average decrease of 7.1+/−5.9%) but did attenuate a secondary dilation that occurs within 20 seconds of a single contraction at specific stimulus frequencies (20, 30 and 40Hz) as well as the dilation 10 seconds following a 60Hz contraction. Thus K + appears to be involved in the rapid dilation in response to a single muscle contraction at all stimulus frequencies while the contribution of ACh is delayed and is stimulus frequency dependent. This work was supported by NSERC.