Wollheim C B, Kikuchi M, Renold A E, Sharp G W
J Clin Invest. 1977 Nov;60(5):1165-73. doi: 10.1172/JCI108869.
The effects of somatostatin and epinephrine have been studied with regard to glucose-induced insulin release and (45)Ca(++) uptake by rat pancreatic islets after 2 days in tissue culture and with regard to (45)Ca(++) efflux from islets loaded with the radio-isotope during the 2 days of culture. (45)Ca(++) uptake, measured simultaneously with insulin release, was linear with time for 5 min. (45)Ca(++) efflux and insulin release were also measured simultaneously from perifused islets. Glucose (16.7 mM) markedly stimulated insulin release and (45)Ca(++) uptake. Somatostatin inhibited the stimulation of insulin release by glucose in a concentration-related manner (1-1,000 ng/ml) but was without effect on the glucose-induced stimulation of (45)Ca(++) uptake. Similarly, under perifusion conditions, both phases of insulin release were inhibited by somatostatin while no effect was observed on the pattern of (45)Ca(++) efflux after glucose.Epinephrine, in contrast to somatostatin, caused a concentration-dependent inhibition of the stimulation of both insulin release and (45)Ca(++) uptake by glucose. Both phases of insulin release were inhibited by epinephrine and marked inhibition could be observed with no change in the characteristic glucose-evoked pattern of (45)Ca(++) efflux (e.g., with 10 nM epinephrine). The inhibitory effect of epinephrine on (45)Ca(++) uptake and insulin release appeared to be mediated via an alpha-adrenergic mechanism, since is was abolished in the presence of phentolamine. Somatostatin inhibits insulin release without any detectable effect upon the handling of calcium by the islets. In contrast, inhibition of insulin release by epinephrine is accompanied by a partial inhibition of glucose-induced Ca(++) uptake.
在组织培养2天后，研究了生长抑素和肾上腺素对大鼠胰岛葡萄糖诱导的胰岛素释放以及（45）Ca（++）摄取的影响，以及在培养的2天期间对加载放射性同位素的胰岛中（45）Ca（++）流出的影响。与胰岛素释放同时测量的（45）Ca（++）摄取在5分钟内与时间呈线性关系。还从灌流的胰岛中同时测量了（45）Ca（++）流出和胰岛素释放。葡萄糖（16.7 mM）显著刺激胰岛素释放和（45）Ca（++）摄取。生长抑素以浓度相关的方式（1 - 1000 ng/ml）抑制葡萄糖对胰岛素释放的刺激，但对葡萄糖诱导的（45）Ca（++）摄取刺激没有影响。同样，在灌流条件下，生长抑素抑制胰岛素释放的两个阶段，而对葡萄糖后（45）Ca（++）流出模式没有影响。与生长抑素相反，肾上腺素导致葡萄糖对胰岛素释放和（45）Ca（++）摄取刺激的浓度依赖性抑制。胰岛素释放的两个阶段都被肾上腺素抑制，并且在（45）Ca（++）流出的特征性葡萄糖诱发模式没有变化的情况下可以观察到明显的抑制（例如，用10 nM肾上腺素）。肾上腺素对（45）Ca（++）摄取和胰岛素释放的抑制作用似乎是通过α - 肾上腺素能机制介导的，因为在酚妥拉明存在下这种作用被消除。生长抑素抑制胰岛素释放，而对胰岛处理钙没有任何可检测到的影响。相比之下，肾上腺素对胰岛素释放的抑制伴随着对葡萄糖诱导的Ca（++）摄取的部分抑制。
