Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism

Objective To study the interaction between autonomic nervous activity and t hyroid hormones in the control of heart rate (HR) and blood pressure (BP). Design and methods Thyrotoxicosis was produced by injections of L-thyroxine (0.5 mg/kg/day for five days). Blockers were atropine (0.5 mg/kg), atenolo l (1 mg/kg) or prazosin (1 mg/kg). Eight animals were studied in each group . Spectral analyses was performed using continuous BP time series obtained in conscious rats. Results Thyroxine treatment was sufficient to induce a significant degree o f tachycardia (423 +/- 6 vs 353 +/- 4 bpm, P < 0.001, unpaired Student's t test), systolic BP elevation (142 +/- 3 vs 127 +/- 2 mmHg, P < 0.001) and c ardiac hypertrophy (1.165 +/- 0.017 vs 1.006 +/- 0.012 g, P < 0.001). The i ntrinsic HR was markedly increased after treatment with thyroxine (497 +/- 16 vs 373 +/- 10 bpm, P < 0.05). Vagal tone was positively linearly related to intrinsic HR (r = 0.84, P < 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyroidism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (modulus 1.10 /- 0.07 vs 1.41 +/- 0.06 mmHg, P < 0.01). Prazosin was without effect on th is 0.4 Hz component in hyperthyroid animals. Conclusions These data show a functional diminution of the vascular and car diac sympathetic tone in early experimental hyperthyroidism. The marked ris e in the intrinsic HR could be the main determinant of tachycardia. The BP elevation may reflexly induce vagal activation and sympathetic (vascular an d cardiac) inhibition. J Hypertens 1998, 16:1989-1992 (C) 1998 Lippincott W illiams & Wilkins.