par Malaisse, Willy 
;Herchuelz, André ;Levy, J.;Sener, Abdullah
Référence Biochemical pharmacology, 26, 8, page (735-740)
Publication Publié, 1977-04
;Herchuelz, André ;Levy, J.;Sener, Abdullah Référence Biochemical pharmacology, 26, 8, page (735-740)
Publication Publié, 1977-04
Article révisé par les pairs
| Résumé : | Verapamil is known to abolish glucose- or sulfonylurea-induced insulin release by the isolated perfused rat pancreas. The mode of action of verapamil upon islet function is investigated. The drug apparently does not interfere with the process of glucose metabolism and recognition by the B-cell, since the utilization and oxidation of glucose, the total production of lactate, the synthesis of proinsulin, and the inhibitory effect of glucose on 45calcium efflux in isolated islets were all unaffected by verapamil. The drug inhibited basal and glucose- or sulfonylurea-stimulated 45calcium net uptake, without facilitating 45calcium efflux from perifused islets. It failed to abolish the increase in both 45calcium efflux and insulin output evoked by theophylline. These data suggest that a major effect of verapamil is to inhibit calcium entry in the B-cell, as if such an influx were to occur, in part at least, through calcium channels analogous to those described in myocardium and myometrium. The proper effect of glucose on calcium handling by the islets was not abolished by verapamil and may, therefore, not require the functional integrity of the system responsible for calcium inward transport in the B-cell. |
