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本文以细胞外K~+刺激、哇巴因不敏感的Na~+内向净增流量(△Na)估计红细胞协同转运功能,通过对30个家系、144人作谱系调查发现:①双亲中一方、双方异常的家系子代△Na异常率与盂德尔理想遗传比值间无显著统计学差异;②在家系的连续三代人中均见有△Na异常者;③△Na频数分布曲线呈现双峰,提示存在两个不同“质”的群体;④受测者△Na值与原发性高血压的发生间经统计学测验关系十分密切。我们认为,按盂德尔显性单基因遗传规律传递的细胞膜协同转运功能缺陷与原发性高血压密切有关。它对预报、预防、遗传分型及鉴别诊断等可能有重要启示。
In this paper, the extracellular K ~ + stimulation, ouabain insensitive Na ~ + inward net increase flow (△ Na) estimated erythrocyte co-transport function, through 30 families, 144 people were pedigree survey found: ① parents in one, There was no statistically significant difference between the abnormal rate of △ Na in the offspring of the two families and the optimal genetic ratio of the Yudel; ②The abnormalities of △ Na were found in all the three generations of pedigrees; ③ The distribution of △ Na frequency showed a double peak, suggesting There are two different “quality” groups; ④ subjects △ Na value and the incidence of essential hypertension by the statistical test between the very close. In our opinion, the defects of cell membrane co-transport function transmitted by the dominant single gene of the mantle are closely related to essential hypertension. It may have important implications for prediction, prevention, genetic typing and differential diagnosis.