Deficient activity of stimulatory nucleotide-binding regulatory protein in lymphocytes from patients with essential hypertension.
Deficient activity of stimulatory nucleotide-binding regulatory protein in lymphocytes from patients with essential hypertension.
复制标题
原发性高血压患者淋巴细胞中刺激性核苷酸结合调节蛋白活性不足。
DOI：
--
复制
发表时间：
1994
影响因子：
3.2
通讯作者：
Y. Masuyama
中科院分区：
文献类型：
--
作者：
H. Yoshikawa;K. Fukuda;Y. Wanaka;K. Kasamatsu;A. Baba;I. Nishio;Y. Masuyama
淋巴细胞被广泛用作心血管β-肾上腺素受体-腺苷酸环化酶系统的模型。我们通过研究从原发性高血压患者中获得的淋巴细胞来评估该系统在高血压发病机制中的作用。未经治疗的高血压患者和血压正常的对照组进行了研究。用125I-氰基吲哚酚放射性配体结合法测定β-肾上腺素受体的数量和亲和力。环磷酸腺苷（cAMP）异丙肾上腺素，霍乱毒素，毛喉素的反应也进行了测定。两组中β-肾上腺素受体的浓度和亲和力没有显著差异，cAMP的基础水平也没有显著差异。异丙肾上腺素对高血压患者淋巴细胞cAMP蓄积的影响较正常血压者明显降低。在两组中，毛喉素对cAMP积累的影响无显著差异。这些结果表明，活性的刺激性核苷酸结合调节蛋白（GS蛋白）降低淋巴细胞从原发性高血压患者。这种淋巴细胞中GS蛋白的缺陷可能代表了此类患者心血管系统中GS蛋白的缺陷。
Lymphocytes are widely used as a model for the cardiovascular beta-adrenoceptor-adenylate cyclase system. We evaluated the role of this system in the pathogenesis of hypertension by studying lymphocytes obtained from patients with essential hypertension. Untreated hypertensive patients and normotensive control subjects were studied. The number and affinity of the beta-adrenoceptors were measured by a radioligand binding method with 125I-cyanopindolol. The responses of cyclic adenosine monophosphate (cAMP) to isoproterenol, cholera toxin, and forskolin were also determined. The concentration and affinity of beta-adrenoceptors did not differ significantly in the two groups, nor was a significant difference found in the basal level of cAMP. The effects of isoproterenol on the accumulation of cAMP were reduced in the lymphocytes from the hypertensive compared with the normotensive subjects. There was no significant difference in the effect of forskolin on cAMP accumulation in the two groups. These results indicate that the activity of the stimulatory nucleotide binding regulatory protein (Gs-protein) is reduced in lymphocytes from patients with essential hypertension. This defect of Gs-protein in the lymphocytes may represent a defect of Gs-protein in the cardiovascular system in such patients.