Acute hyperthyroidism alters adrenoceptor- and muscarinic receptor-mediated responses in isolated rat renal and femoral arteries

Abstract

The effects of acute hyperthyroidism on the vasorelaxing responses to isoprenaline and acetylcholine were investigated in isolated rat renal and femoral arteries. In the renal artery, isoprenaline- and acetylcholine-induced relaxations were significantly greater in hyperthyroid rats than in control rats. In the femoral artery, only the acetylcholine-induced relaxation was significantly greater in hyperthyroid rats than in control rats. In the renal artery, N G-nitro- l-arginine ( l-NOARG), an inhibitor of nitric oxide (NO) synthase, reduced isoprenaline- and acetylcholine-induced relaxations in both hyperthyroid and control rats and the isoprenaline-induced relaxation was still greater in hyperthyroid rats than in control rats, but no difference in the acetylcholine-induced relaxation was seen between the two groups of rats since l-NOARG almost abolished the acetylcholine-induced relaxation. In the femoral artery, l-NOAGR reduced the isoprenaline-induced relaxation in control rats but not in hyperthyroid rats, while it almost abolished the acetylcholine-induced relaxation in both groups of rats. 17-Octadecynoic acid (17-ODYA), a cytochrome P-450 monooxygenase inhibitor, reduced the isoprenaline-induced relaxation in renal and femoral arteries from hyperthyroid and control rats, but it did not change the acetylcholine-induced relaxation in both arteries. These results indicate that acute hyperthyroidism significantly enhances β-adrenoceptor-mediated relaxation of the renal artery and muscarinic receptor-mediated relaxation of both renal and femoral arteries, suggesting that these effects may be due to an alteration in the NO and cytochrome P-450 systems of the artery.