Regulation of calcium fluxes in rat pancreatic islets: the role of K+ conductance.
The effects of tetraethylammonium (TEA), a specific blocker of K+ conductance, on calcium fluxes and insulin release in isolated islets were investigated in order to explore the possible relevance of changes in K+ conductance to the mechanism by which glucose both decreases Ca fractional outflow rate from and stimulates Ca entry into the beta-cell. TEA reduced 86Rb efflux from prelabeled islets to the same extent as a non-insulinotropic glucose concentration. In the absence of glucose, TEA failed to affect 45Ca fractional outflow rate, 45Ca net uptake and insulin release from isolate islets. The drug lowered the threshold concentration of glucose required to stimulate these parameters and dramatically increased the cationic and secretory responses to intermediate glucose concentrations. The effect of TEA was less marked at a high glucose concentration. In the absence or presence of TEA, the effect of glucose to stimulate 45Ca efflux required the presence of extracellular calcium. It is concluded that TEA by inhibiting K+ conductance mimics to a limited extent the effect of glucose in causing the gating of voltage-sensitive calcium channels in isolated islets. The inhibitory effect of glucose upon Ca outflow rate, however, appears unrelated to changes in K+ conductance.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*
D007328:Insulin; D013757:Tetraethylammonium Compounds; D005947:Glucose; D011188:Potassium; D002118:Calcium