Nunez A M, Devynck M A, Meyer P
J Neurochem. 1982 May;38(5):1342-7. doi: 10.1111/j.1471-4159.1982.tb07911.x.
A large number (about 4--5 nmol/mg of protein) of high-affinity (apparent dissociation constant at 37 degrees C: KD37 degrees C = 5 x 10(-8) M) calcium binding sites was characterized in synaptosomal membrane fractions enriched in plasma membranes that were isolated from rat brain. These sites were studied simultaneously in membranes from spontaneously hypertensive young rats (SHR) and their normotensive controls. No difference was observed between whole synaptosomes from these two substrains. However, plasma membrane-enriched fractions from SHR exhibited a reduced calcium binding capacity without a significant change in affinity. This decrease which averaged 15--20% was not due to any variation in the accessibility of calcium to its binding sites, as similar results were obtained in the presence of the calcium ionophore A23187. The reduction found in calcium binding is very similar to that previously described in erythrocyte membranes. It is envisaged that such an abnormality at nerve endings might play a role in the pathogenesis of genetic hypertension.
在从大鼠脑中分离出的富含质膜的突触体膜组分中，鉴定出大量（约4 - 5 nmol/mg蛋白质）高亲和力（37℃时的表观解离常数：KD37℃ = 5×10⁻⁸ M）的钙结合位点。同时对自发性高血压幼鼠（SHR）及其血压正常的对照鼠的膜进行了研究。这两个亚系的全突触体之间未观察到差异。然而，SHR富含质膜的组分表现出钙结合能力降低，而亲和力没有显著变化。这种平均降低15 - 20%的情况并非由于钙与其结合位点的可及性存在任何差异，因为在钙离子载体A23187存在的情况下也获得了类似结果。钙结合的减少与先前在红细胞膜中描述的情况非常相似。据推测，神经末梢的这种异常可能在遗传性高血压的发病机制中起作用。
