Swann A C
Department of Psychiatry, University of Texas Medical School, Houston 77225.
Eur J Pharmacol. 1989 Oct 10;169(2-3):275-83. doi: 10.1016/0014-2999(89)90025-3.
We investigated interactions between noradrenaline and thyroid hormone status in the regulation of (Na+,K+)-ATPase in vivo. Treatment with the beta-adrenoceptor antagonist propranolol or with the neurotoxin 6-hydroxydopamine did not prevent the increases in heart (Na+,K+)-ATPase associated with triiodothyronine treatment. Administration of methimazole did not prevent the increase in (Na+,K+)-ATPase indices in cerebral cortex and heart associated with subacute noradrenergic stimulation by yohimbine. There was no evidence for synergistic effects between thyroid hormone administration and noradrenergic stimulation by yohimbine. Thyroid hormone, unlike noradrenaline, mainly increased (Na+,K+)-ATPase activity with low affinity for ouabain. These results show that noradrenaline and thyroid hormone regulate (Na+,K+)-ATPase by largely independent mechanisms, and may regulate different populations of enzyme molecules.
我们研究了去甲肾上腺素与甲状腺激素状态在体内对(Na⁺,K⁺)-ATP酶调节中的相互作用。用β-肾上腺素能受体拮抗剂普萘洛尔或神经毒素6-羟基多巴胺进行处理,并不能阻止与三碘甲状腺原氨酸处理相关的心脏(Na⁺,K⁺)-ATP酶增加。给予甲巯咪唑并不能阻止与育亨宾亚急性去甲肾上腺素能刺激相关的大脑皮质和心脏中(Na⁺,K⁺)-ATP酶指数增加。没有证据表明甲状腺激素给药与育亨宾去甲肾上腺素能刺激之间存在协同作用。与去甲肾上腺素不同,甲状腺激素主要以对哇巴因低亲和力的方式增加(Na⁺,K⁺)-ATP酶活性。这些结果表明,去甲肾上腺素和甲状腺激素通过很大程度上独立的机制调节(Na⁺,K⁺)-ATP酶,并且可能调节不同群体的酶分子。