ROLE OF NITRIC-OXIDE IN THE SYSTEMIC CIRCULATION OF CONSCIOUS HYPERTHYROID AND HYPOTHYROID RATS

1. N-omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO biosynthesis, which blocks basal NO production, caused a similar incre ase of mean arterial pressure (MAP) in control hyper- and hypothyroid rats at the lowest dose, however, smaller pressor effects were observe d with increasing doses in hyper- and hypothyroid rats. An additional dose of L-NAME (30 mg/kg), which produced no further increase in press ure, killed 90% of the hyperthyroid rats, whereas hypothyroid and cont rol rats survived this additional dose. 2. The systemic responses to a cetylcholine (ACh), an endothelium-dependent vasodilator that stimulat es NO production/release, were significantly increased in hypothyroid rats, while hyperthyroid rats showed no significant differences when c ompared with controls. However, 10(-8) M ACh killed hyperthyroid rats, whereas control and hypothyroid rats survived this dose. 3. The maxim al hypotensive response to sodium nitroprusside (SNP), an agonist that generates NO, was similar in intact controls, hyper- and hypothyroid rats. 4. These data indicate that hyper- and hypothyroidism show a red uction in basal NO synthesis/release, this reduced systemic NO tone be ing essential for life in hyperthyroid rats; whereas the response to A Ch is not reduced and the hypotensive response to SNP did not differ b etween groups, indicating that the responsiveness of the systemic circ ulation to NO is not altered in either thyroid disorder.