Abstract
Historic studies with sodium ion (Na+) micropipettes and firstâgeneration fluorescent probes suggested that an increase in heart rate results in higher intracellular Na+âlevels. Using a dual fluorescence indicator approach, we simultaneously assessed the dynamic changes in intracellular Na+ and calcium (Ca2+) with measures of force development in isolated excitable myocardial strip preparations from rat and human left ventricular myocardium at different stimulation rates and modeled the Na+âeffects on the sodiumâcalcium exchanger (NCX). To gain further insight into the effects of heart rate on intracellular Na+âregulation and sodium/potassium ATPase (NKA) function, Na+, and potassium ion (K+) levels were assessed in the coronary effluent (CE) of paced human subjects. Increasing the stimulation rate from 60/min to 180/min led to a transient Na+âpeak followed by a lower Na+âlevel, whereas the return to 60/min had the opposite effect leading to a transient Na+âtrough followed by a higher Na+âlevel. The presence of the Na+âpeak and trough suggests a delayed regulation of NKA activity in response to changes in heart rate. This was clinically confirmed in the pacing study where CEâK+ levels were raised above steadyâstate levels with rapid pacing and reduced after pacing cessation. Despite an initial Na+ peak that is due to a delayed increase in NKA activity, an increase in heart rate was associated with lower, and not higher, Na+âlevels in the myocardium. The dynamic changes in Na+ unveil the adaptive role of NKA to maintain Na+ and K+âgradients that preserve membrane potential and cellular Ca2+âhemostasis.
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