Abstract
In quiescent papillary muscles isolated from hearts of rats with streptozotocin-induced diabetes resting intracellular sodium activity (aiNa) was about 56% greater than in muscles from controls. An intracellular acid load induced by the NH4+ method caused a rise in aiNa whose maximum amplitude was similar in both groups of muscles. However, the half-time to maximum amplitude was increased by about 56% in diabetic muscles. These results are consistent with a diabetes-induced decrease in the activity of the sarcolemmal Na(+)-H+ exchange.
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