Limlomwongse L, Krishnamra N
Proc Soc Exp Biol Med. 1981 Oct;168(1):72-6. doi: 10.3181/00379727-168-41237.
The hypocalcemia effect of gastrin and the possible role of the hormone in calcium homeostasis have been demonstrated in our previous study. The mechanism involves neither the gastrointestinal absorption nor the removal of calcium from plasma but is possibly due to the suppression of the calcium influx into blood. In searching for the organ(s) involved in the action of gastrin, the following were tested and not found to be directly responsible: stomach, intestine, pancreas, liver, spleen, adrenal gland, kidney, lung, muscle, and red blood cell. After 17 hr of 45Ca administration, the turnover of 45Ca in the tibia was measured. Gastrin was found to suppress the release of 45Ca by 25% within 1 hr. The suppressive effect of gastrin on 45Ca release was also demonstrated in an in vitro preparation which showed that the 45Ca released from prelabeled tibia into the incubating medium was also reduced by gastrin. It was thus concluded that the gastrin-induced hypocalcemia in rat was the result of a suppression of the release of calcium from bone.
胃泌素的低钙血症效应以及该激素在钙稳态中的可能作用已在我们之前的研究中得到证实。其机制既不涉及胃肠道对钙的吸收,也不涉及从血浆中清除钙,而可能是由于抑制了钙流入血液。在寻找参与胃泌素作用的器官时,对以下器官进行了测试,发现它们并非直接原因:胃、小肠、胰腺、肝脏、脾脏、肾上腺、肾脏、肺、肌肉和红细胞。给予45Ca 17小时后,测量胫骨中45Ca的周转率。发现胃泌素在1小时内可抑制45Ca的释放25%。胃泌素对45Ca释放的抑制作用在体外实验中也得到了证实,该实验表明,预先标记的胫骨释放到培养液中的45Ca也会被胃泌素减少。因此得出结论,大鼠中胃泌素诱导的低钙血症是骨钙释放受抑制的结果。