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)
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