Scarpace P J, Abrass I B
Endocrinology. 1981 Apr;108(4):1276-8. doi: 10.1210/endo-108-4-1276.
To evaluate the capacity of the myocardium in aged rats to respond to hyperthyroidism, we quantified myocardial beta-adrenergic receptors in female Fischer 344 rats of 3, 12, and 24 months of age. In T3-treated rats (500 microgram T3/kg . day for 3 days), myocardial beta-adrenergic receptors, as measured by [3H]dihydroalprenolol binding, were significantly increased (P less than 0.01) over controls in 3-, 12-, and 24-month-old animals. The data demonstrate that senescent rats retain the capacity to increase myocardial beta-adrenergic receptors in response to exogenous hyperthyroidism. In the myocardium, the mechanism of decreased catecholamine responsiveness in aging appears to be at other than the beta-adrenergic receptor site, since receptor density is unaltered with age, as is receptor modulation in response to hyperthyroidism.
为评估老年大鼠心肌对甲状腺功能亢进的反应能力,我们对3个月、12个月和24个月大的雌性Fischer 344大鼠的心肌β-肾上腺素能受体进行了定量分析。在接受T3治疗的大鼠中(500微克T3/千克·天,持续3天),通过[3H]二氢阿普洛尔结合法测定,3个月、12个月和24个月大动物的心肌β-肾上腺素能受体较对照组显著增加(P<0.01)。数据表明,衰老大鼠保留了对外源性甲状腺功能亢进作出反应增加心肌β-肾上腺素能受体的能力。在心肌中,衰老过程中儿茶酚胺反应性降低的机制似乎并非位于β-肾上腺素能受体部位,因为受体密度不会随年龄而改变,对甲状腺功能亢进的受体调节也是如此。