Catecholamines and thyroid hormones have a similar influence on heart function and metabolism, but this may occur in a differential manner and to a different extent In this study, the effects of norepinephrine (NE) and of triiodothyronine (T₃) were studied in regard to the function of the left (LV) and right ventricle (RV) and to the oxidative pentose phosphate pathway (PPP). NE was applied in rats as continuous i. v. infusion (0.2 mg/kg/h) for three days. T₃ was given as daily s.c. injections (0.2 mg/kg) for the same period of time. LV, and RV function was measured in the closed-chest trapanal-anesthetized animals using special Millar ultraminature catheter pressure transducers. NE induced an increase in heart rate, in mean arterial pressure, and in total peripheral resistance (TPR). The cardiac RNA/DNA and the left ventricular weight/body weight ratios were increased by about 40%. These effects were prevented by simultaneous α-and β-receptor blockade with prazosin and metoprolol, respectively, but not by verapamil which abolished the hemodynamic effects. RVSP was significantly elevated by NE in a dose-dependent manner. The functional effects of T₃ on the LV were not as pronounced as those induced by NE. Heart rate and LV dp/dt_max were increased by T₃ and this increase was prevented by concomitant β-receptor blockade with, metoprolol. In contrast to NE, T₃ induced an increase in cardiac output and a concominant decrease in TPR. The RNA/DNA ratio was elevated and cardiac hypertrophy had developed after treatment for three days with T₃. These changes were not affected by β-receptor blockade with metoprolol. RVSP was increased by T₃ to a lesser extent than with NE. In metabolic terms in turned out that only NE, but not T₃ had a stimulating effect on the cardiac PPP. NE increased the mRNA and activity of glucose-6-phosphate dehydrogenase (G-6-PD), the first and regulating enzyme of this pathway. However, there was no effect of T₃ on G-6-PD activity nor on 6-phosphogluconate dehydrogenase activity, one of the following enzymes in the pathway within the first 5 days of T₃ treatment. These results demonstrate that the functional effects of T₃ were not as pronounced as or even different from those of NE, and that T₃ lacked a stimulating effect on the cardiac PPP.

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