Effects of triiodothyronine in spontaneously hypertensive rats. Studies on cardiac metabolism, function, and heart weight

Summary

We have studied the effects of triiodothyronine (T₃) on heart function,on the myocardial oxidative pentose phosphate pathway, and on heart weight in spontaneously hypertensive (SHR) rats. Another aim was to examine whether these T₃-effects may be reversible. T₃ was administered daily (0.2 mg/kg s. c.) for 14 days. Compared to the untreated SHR controls, T₃ induced an increase in heart rate (beast/min) from 357±10 (n=17) to 553±10 (n=17), in the pressure-rate-product (mm Hg/min) from 78400±4500 (n=15) to 113700±4800 (n=15), and in the heart weight/body weight ratio (mg/g) from 4.2±0.2 (n=20) to 5.8±0.2 (n=19). The activity of myocardial glucose-6-phosphate dehydrogenase, the first and rate-limiting enzyme of the oxidative pentose phosphate pathway (units/g protein), was clevated from 4.2±0.2 (n=9) to 7.0±0.6 (n=9) after 14 days of T₃-treatment while the activity of 6-phosphogluconate dehydrogenase, one of the following enzymes in the pathway, was not altered appreciably. These changes returned to the respective control values when T₃-treatment was discontinued for 14 days. Our results demonstrate that T₃ had a positive chronotropic effect and induced an additional heart enlargement in an animal model with already established cardiac hyperfunction and hypertrophy. The effects on heart function and weight, which were fully reversible, were not as pronounced as in normal Sprague-Dawley rats.