Marre M, Gauville C, Passa P
Arch Mal Coeur Vaiss. 1985 Oct;78(11):1661-6.
Insulin release is coupled with a calcium entry into the pancreatic B cells. The use of calcium-antagonists may eventually alter glucose homeostasis. To evaluate this possibility, nicardipine action was tested both in vitro and in vivo: 1. on insulin release and vascular resistances from isolated perfused rat pancreases; 2. on 7 hypertensive patients with an established glucose intolerance, during two oral glucose tolerance tests (OGTT) performed successively under placebo and nicardipine (90 mg daily) at a two-week interval. In vitro, the basal insulin release from isolated perfused rat pancreases (86 +/- 15 ng.min-1; n = 27; M +/- SE) was inhibited according to the nicardipine dose by the 5 th min. of infusion: 7.2 +/- 1.5 p.100 of the initial output at 10(-4) M (n = 6; p less than %.001); 33.4 +/- 2.7 p.100 at 10(-6) M (n = 6; p less than 0.001); 87.5 +/- 14.8 p.100 at 10(-8) M (n = 6; ns). The pancreatic vascular resistances declined significantly for the 3 doses, but no dose-response could be registered. In vivo, the mean arterial blood pressure was significantly reduced by nicardipine from 114 +/- 3 mmHg to 95 +/- 3 mmHg (p less than 0.001) without any significant alteration of either glucose tolerance (glycaemias at the 120 th min of OGTT: 9.2 +/- 1.1 mmol.l-1 vs 8.9 +/- 1.2 mmol.-1) or insulin peak: 70 +/- 20 micrograms U.ml-1 vs 67 +/- 22 microU.ml-1.(ABSTRACT TRUNCATED AT 250 WORDS)
胰岛素释放与钙离子进入胰腺β细胞相偶联。使用钙拮抗剂最终可能会改变葡萄糖稳态。为评估这种可能性，在体外和体内对尼卡地平的作用进行了测试：1. 对分离灌注的大鼠胰腺的胰岛素释放和血管阻力的影响；2. 对7名已确诊糖耐量异常的高血压患者，在间隔两周先后进行的两次口服葡萄糖耐量试验（OGTT）中，先服用安慰剂，后服用尼卡地平（每日90毫克）。在体外，从分离灌注的大鼠胰腺释放的基础胰岛素（86±15纳克·分钟-1；n = 27；平均值±标准误）在输注第5分钟时根据尼卡地平剂量受到抑制：在10(-4)M时为初始输出的7.2±1.5%（n = 6；p<0.001）；在10(-6)M时为33.4±2.7%（n = 6；p<0.001）；在10(-8)M时为87.5±14.8%（n = 6；无显著差异）。胰腺血管阻力在3个剂量下均显著下降，但未观察到剂量反应关系。在体内，尼卡地平使平均动脉血压从114±3毫米汞柱显著降至95±3毫米汞柱（p<0.001），而葡萄糖耐量（OGTT第120分钟时的血糖：9.2±1.1毫摩尔/升对8.9±1.2毫摩尔/升）或胰岛素峰值（70±20微单位/毫升对67±22微单位/毫升）均无显著改变。（摘要截取自250字）
