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J Appl Physiol 90: 2063-2069, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 6, 2063-2069, June 2001

Renal hypertension prevents run training modification of cardiomyocyte diastolic Ca2+ regulation in male rats

Bradley M. Palmer, Joshua M. Lynch, Steven M. Snyder, and Russell L. Moore

Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder, Colorado 80309

The combined effects of endurance run training and renal hypertension on cytosolic Ca2+ concentration ([Ca2+]c) dynamics and Na+-dependent Ca2+ regulation in rat left ventricular cardiomyocytes were examined. Male Fischer 344 rats underwent stenosis of the left renal artery [hypertensive (Ht), n = 18] or a sham operation [normotensive (Nt), n = 20]. One-half of the rats from each group were treadmill trained for >16 wk. Cardiomyocyte fura 2 fluorescence ratio transients were recorded for 7 min during electrical pacing at 0.5 Hz, 2 mM extracellular Ca2+ concentration, and 29°C. The rate of [Ca2+]c decline was not changed by run training in the Nt group but was reduced in the Ht group. At 7 min, cardiomyocytes were exposed to 10 mM caffeine in the absence of Na+ and Ca2+, which triggered sarcoplasmic reticular Ca2+ release and suppressed Ca2+ efflux via Na+/Ca2+ exchanger. External Na+ was then added, and Na+-dependent Ca2+ efflux rate was recorded. Treadmill training significantly enhanced Na+-dependent Ca2+ efflux rate under these conditions in the Nt group but not in the Ht group. These data provide evidence that renal hypertension prevents the normal run training-induced modifications in diastolic [Ca2+]c regulation mechanisms, including Na+/Ca2+ exchanger.

sodium ion/calcium ion exchange; sodium ion/calcium ion exchanger; fura 2; sarcoplasmic reticulum; treadmill


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