| Abstrakt: |
Summary In hypothyroid rat myocardium, the low-ouabain-sensitivity Na,K-ATPase activity had aKi=10-4m and accounted for ~95% of the enzyme activity, while the high-ouabain-sensitivity activity contributed ~5% to the total activity, with aKi=3×107m. mRNAa1 was 7.2- and 5.5-fold more abundant than mRNAa2 and mRNAß, respectively, in hypothyroid ventricles while mRNAa3 was undetectable. Administration of T3 increased total Na,K-ATPase activity 1.6-fold; the low-ouabain-sensitivity activity increased 1.5-fold while high-ouabain-sensitivity activity was stimulated 3.2-fold. T3 increased the number of high-affinity ouabain-binding sites 2.9-fold with no change inKd (~2×10-7m). The abundances of mRNAa1, mRNAa2, and mRNAß (per unit RNA) following T3 treatment increased 3.6-, 10.6-, and 12.7-fold, respectively. The larger increments in subunit mRNA abundances than in Na,K-ATPase activity suggests the involvement of translational and/or post-translational regulatory steps in Na,K-ATPase biogenesis in response to T3. It is concluded that T3 enhances myocardial Na,K-ATPase subunit mRNA abundances and Na,K-ATPase activity, and that the expression of the high- and low-ouabain-sensitivity activities are probably a reflection of the abundances of the a2 and a1 isoforms, respectively. The physiological role played by the ß subunit remains uncertain. |
Full text from SpringerLink