Troponin I and T protein expression in experimental cardiac hypertrophy.

We have examined four models of experimental cardiac hypertrophy and heart failure for alterations in troponin isoform expression, particularly in the re-expression of the fetal isoforms. Cardiac protein extracts from experimental and sham-operated control rats were analyzed using one dimensional gel electrophoresis, followed by Western blotting and detection with antibodies specific for troponin I and T. No alteration in protein profile was observed for these proteins between control, hypertrophied and failing heart samples. The data demonstrate that reversion to the fetal pattern of troponin expression is not a feature of experimental cardiac hypertrophy and heart failure in the rat.

Skeletal muscle metabolism in uremic rats: a 31P-magnetic resonance study.

The effect of uremia on skeletal muscle metabolism of the rat was examined using 31P-magnetic resonance spectroscopy. Three weeks following either a 5/6 nephrectomy or a sham operation, Wistar rats were placed in a 7T magnet, and the sciatic nerve was stimulated for 10 min. Analysis of spectra allowed calculation of intracellular pH and the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi) and ATP. [ADP] was calculated from the creatine kinase equilibrium. There was a significant reduction in the resting intracellular [Pi] despite an elevation in extracellular [Pi], probably due to a reduction in the activity of the membrane Na/Pi cotransporter on account of a reduced sodium gradient. Despite anemia and uremia, there were no significant metabolic abnormalities during exercise and recovery accompanying this substantial reduction in glomerular filtration rate implying that at this level of renal impairment, there is no mitochondrial dysfunction.