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甲状旁腺钙受体 (CaR)是与G蛋白相偶联的膜受体。胞外Ca2 + 通过激活CaR ,可快速、独立地影响甲状旁腺激素 (PTH)的分泌。慢性肾功能衰竭 (肾衰 )继发甲状旁腺功能亢进 (甲旁亢 )时 ,Ca调定点升高 ,PTH过度分泌。多数学者认为这与甲状旁腺CaR的mRNA表达下降及受体蛋白合成减少有关 ,而与CaR的基因突变无关。CaR的激动剂能模仿甚至增强胞外Ca2 + 对甲状旁腺细胞的效应 ,初步证实它能快速、安全、有效地抑制PTH分泌 ,延缓肾性骨病的发展。
Parathyroid calcium receptor (CaR) is a membrane receptor that is coupled to the G protein. Extracellular Ca2 + can rapidly and independently affect the secretion of parathyroid hormone (PTH) by activating CaR. Chronic renal failure (renal failure) secondary to hyperparathyroidism (hyperparathyroidism), Ca set point increased, PTH over-secretion. Most scholars believe that this parathyroid CaR mRNA expression decreased receptor protein synthesis and reduced, and CaR gene mutation has nothing to do. CaR agonists can mimic and even enhance the effect of extracellular Ca2 + on parathyroid cells, initially confirming that it can rapidly, safely and effectively inhibit PTH secretion and delay the development of renal osteodystrophy.