Abstract
We tested the hypothesis that the negative functional effects of cyclic GMP were mediated by ryanodine receptors, and that these effects would be reduced in thyroxine (thyroxine, 0.5 mg/kg/day, 16 days)-induced hypertrophic myocytes. Using rabbit ventricular myocytes from control (n=9) and thyroxine (n=9) hearts, percent cell shortening (%) and maximum rate of contraction and relaxation were determined using a video edge detector at baseline and after 10(-6), 10(-5) M 8-bromo-cyclic GMP. Dantrolene 10(-6) M, ryanodine receptor inhibitor, was added alone or after 8-Br-cGMP treatment. Changes in cytosolic Ca(2+) concentration were assessed in fura-2-loaded control and thyroxine myocytes. 8-Br-cGMP caused a significant decrease in percent shortening, from 5.3+/-0.9% to 3.9+/-0.6% at 10(-5 )M in control, and 3.4+/-0.3% to 2.6+/-0.4% in thyroxine myocytes. Dantrolene significantly decreased percent shortening from 4.5+/-0.8% to 3.7+/-0.1% in control and from 3.7+/-0.1% to 2.8+/-0.3% in thyroxine myocytes. In 8-Br-cGMP treated control myocytes, dantrolene did not significantly change myocyte contractility, which suggested that cyclic GMP acted on ryanodine receptors. However, in 8-Br-cGMP treated thyroxine myocytes, dantrolene furthe...Continue Reading
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