Kinin peptides in human trapezius muscle during sustained isometric contraction and their relation to pain.

To determine the muscular concentration of bradykinin and kallidin during static contraction, microdialysis probes were implanted bilaterally in the trapezius muscles of healthy women. Three hours after probe implantation, 200 microM of the angiotensin-converting enzyme (ACE) inhibitor enalaprilat were added to the perfusion solution in one of the sides for 30 min. Thirty minutes later, the subjects performed a sustained bilateral shoulder abduction at 10% of the maximal voluntary contraction until exhaustion. This protocol was repeated twice, with an interval of at least 17 days. High intersession repeatability was observed in the concentration of bradykinin but not of kallidin. Enalaprilat induced a significant increase in bradykinin levels in the dialysate, without affecting kallidin levels. The sustained contraction induced a significant increase in dialysate levels of both kinin peptides. The contraction also induced a significant increase in pain ratings, as measured by a visual analog scale. During contraction, positive correlations were found between pain ratings and levels of kinin peptides in dialysate, predominantly in the side previously perfused with enalaprilat. Subjects with the higher pain ratings also showed larger increases in kinin peptides in the side previously perfused with enalaprilat. The present results show that both plasma and tissue kinin-kallikrein are activated during muscle contraction, but that their metabolic pathways are differently regulated during rest and contraction, because they showed a different response to ACE inhibition. They also indicate that intramuscular kinin peptides levels, and ACE activity, may contribute to muscle pain.