Administration of renin-angiotensin system or sympathetic nervous system blockers prevented thyroxine-induced increases in heart weight and myocyte width in male Wistar rats.
Does inhibition of the renin-angiotensin system or sympathetic nervous system prevent thyroxine-induced cardiac hypertrophy in rats?
Thyroxine-induced cardiac hypertrophy in rats is mediated by both the sympathetic nervous system and the renin-angiotensin system, as blockade of either pathway prevents myocyte remodeling.
The present study assessed the possible involvement of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) in thyroxine (T4)-induced cardiac hypertrophy. Hemodynamic parameters, heart weight (HW), ratio of HW to body weight (HW/BW), and myocyte width were evaluated in absence of thyroid hormone (hypothyroidism) and after T4 administration. Male Wistar rats were used. Some were subjected to thyroidectomies, whereas hyperthyroidism was induced in others via daily intraperitoneal injection of T4 (25 or 100 microg x 100 g BW(-1) x day(-1)) for 7 days. In some cases, T4 administration was combined with the angiotensin I-converting enzyme inhibitor enalapril (Ena), with the angiotensin type 1 (AT1) receptor blocker losartan (Los) or with the beta-adrenergic blocker propanolol (Prop). Hemodynamics and morphology were then evaluated. Systolic blood pressure (SBP) was not altered by administration of either T4 alone or T4 in combination with the specific inhibitors. However, SBP decreased significantly in hypothyroid rats. An increased heart rate was seen after administration of either T4 alone or T4 in combination with either Los or Ena. Although the higher dose of T4 significantly increased HW, HW/BW increased in both T4-treated groups. Ena and Prop inhibited the increase in HW or HW/BW in hyperthyroid rats. Morphologically, both T4 dose levels significantly increased myocyte width, an occurrence prevented by RAS or SNS blockers. There was a good correlation between changes in HW/BW and myocyte width. These results indicate that T4-induced cardiac hypertrophy is associated with both the SNS and the RAS.
Hu et al. (Mon,) conducted a other in Thyroxine-induced cardiac hypertrophy. Thyroxine (T4) alone or combined with enalapril, losartan, or propranolol vs. Hypothyroidism (thyroidectomy) or baseline was evaluated on Hemodynamic parameters, heart weight (HW), HW/BW ratio, and myocyte width. Administration of renin-angiotensin system or sympathetic nervous system blockers prevented thyroxine-induced increases in heart weight and myocyte width in male Wistar rats.