Hyperthyroidism was induced by
subcutaneous injections of
L-thyroxine (T4) (0.5 mg/kg/day) for 3 days in order to investigate the effects of acute
hyperthyroidism on the vasorelaxing responses to
isoprenaline and
acetylcholine in isolated rat aortae. In the aortae, there was no significant difference in
isoprenaline-induced relaxation between
hyperthyroid and control rats, however
acetylcholine-induced relaxation was significantly greater in
hyperthyroid rats than in control rats. 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 in the presence of L-
NOARG no significant difference in the
acetylcholine-induced relaxation was seen between the two groups of rats.
Indomethacin, a
cyclo-oxygenase inhibitor, had no significant influence on both
isoprenaline- and
acetylcholine-induced relaxations in both control and
hyperthyroid rats.
17-Octadecynoic acid (17-ODYA), a
cytochrome P-450 mono-
oxygenase inhibitor, reduced the both
isoprenaline- and
acetylcholine-induced relaxation in both
hyperthyroid and control rats, and
acetylcholine-induced relaxation was still greater in
hyperthyroid rats than in control rats. These results indicate that an acute
hyperthyroidism significantly enhances
muscarinic receptor- but not
adrenoceptor-mediated relaxations of the aortae and L-
NOARG abolished an enhancement by acute
hyperthyroidism of
muscarinic receptor-mediated relaxation, suggesting that the effects may be due to an alteration in
muscarinic receptor-mediated NO systems of the aortae at early stage of
hyperthyroidism.