Ishikawa Y, Gee M V, Ambudkar I S, Bodner L, Baum B J, Roth G S
Molecular Physiology and Genetics Section, National Institute on Aging, Francis Scott Key Medical Center, Baltimore, MD 21224.
Biochim Biophys Acta. 1988 Feb 22;968(2):203-10. doi: 10.1016/0167-4889(88)90009-2.
Alpha 1-Adrenergic-stimulated calcium efflux from rat parotid cell aggregates declines approx. 40% between 3 and 24 months of age, with the bulk of the reduction occurring between 12 and 24 months. Intracellular free calcium levels following alpha 1-adrenoceptor stimulation are also reduced about 40% between 3 and 24 months. No significant age differences in stimulation of inositol mono-, bis- or trisphosphate production are observed. However, the ability of inositol trisphosphate to directly stimulate calcium efflux is reduced by about 50% with increasing age. Concentrations of this inositol phosphate required for maximal calcium release do not change between 3 and 24 months. Differences in response are not due to a reduction in uptake of inositol trisphosphate into older cells, but suggest an age-related defect in the ability of inositol trisphosphate to liberate calcium from intracellular stores. Such dysfunction may be at least partially responsible for impaired alpha 1-adrenergic responsiveness during aging.
α1 - 肾上腺素能刺激引起的大鼠腮腺细胞聚集体钙外流在3至24月龄之间下降约40%,大部分下降发生在12至24月龄之间。α1 - 肾上腺素能受体刺激后的细胞内游离钙水平在3至24月龄之间也降低约40%。未观察到肌醇单磷酸、双磷酸或三磷酸生成刺激方面的显著年龄差异。然而,随着年龄增长,肌醇三磷酸直接刺激钙外流的能力降低约50%。3至24月龄之间,最大钙释放所需的这种肌醇磷酸浓度没有变化。反应差异并非由于老年细胞对肌醇三磷酸摄取减少,而是提示肌醇三磷酸从细胞内储存释放钙的能力存在与年龄相关的缺陷。这种功能障碍可能至少部分导致衰老过程中α1 - 肾上腺素能反应受损。