The aim of the present study was to examine the contribution of intracellular and extracellular calcium sources in contraction caused by noradrenaline (NA) of the human internal thoracic artery (ITA) in vitro. Distal segments of ITA were obtained from 20 patients (aged 38–73, at the time of routine coronary artery surgical revascularization (CABG)). Contractile responses to 10−6 mol/L NA in the physiological salt solution and in Ca2+-free solution without and after incubation with 10−6 mol/L thapsigargin (TSG) were recorded under isometric conditions. Responses of ITA rings to 1 μM NA without incubation with TSG accounted (% of reaction to 80 mM KCl) 224.70 ± 14.06% in PSS solution, 141.30 ± 8.66% in Ca2+-free solution, and 80.03 ± 1.71% after PSS restoration and were statistically significantly different (p < 0.0001, one-way ANOVA). Responses of ITA rings to 1 μM NA with 1 μM TSG accounted (% of reaction to 80 mM KCl) 114.50 ± 2.79% in Ca2+-free solution and 36.70 ± 2.38% after PSS restoration. Responses in Ca2+-free solution and after PSS restoration without and with TSG were statistically significantly different (p = 0.0257 and p < 0.0001, respectively—t test). ITA contraction is caused by calcium derived not only from the SR and the extracellular matrix. The delivery of calcium to the space surrounding tissue does not immediately deliver calcium to the myofilaments.
Pflügers Archiv European Journal of Physiologyl of Physiology – Springer Journals
Published: Apr 22, 2017
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