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

The combined effects of endurance run training and renal hypertension on cy tosolic Ca2+ concentration ([Ca2(+)](c)) dynamics and Na+-dependent Ca2+ re gulation 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 rat s from each group were treadmill trained for >16 wk. Cardiomyocyte fura 2 f luorescence ratio transients were recorded for 7 min during electrical paci ng at 0.5 Hz, 2 mM extracellular Ca2+ concentration, and 29 degreesC. The r ate of [Ca2+](c) decline was not changed by run training in the Nt group bu t 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 re ticular Ca2+ release and suppressed Ca2+ efflux via Na+/Ca2+ exchanger. Ext ernal Na+ was then added, and Na+-dependent Ca2+ efflux rate was recorded. Treadmill training significantly enhanced Na+-dependent Ca2+ efflux rate un der these conditions in the Nt group but not in the Ht group. These data pr ovide evidence that renal hypertension prevents the normal run training-ind uced modifications in diastolic [Ca2+](c) regulation mechanisms, including Na+/Ca2+ exchanger.