A. Berts et al., CYTOPLASMIC CA2-PRODUCING PANCREATIC ALPHA-CELLS EXPOSED TO CARBACHOLAND AGENTS AFFECTING NA+ FLUXES( IN GLUCAGON), Endocrine, 6(1), 1997, pp. 79-83
The cytoplasmic Ca2+ concentration ([Ca2+](i)) was measured with dual
wavelength fluorometry in glucagon-producing mouse pancreatic alpha-ce
lls loaded with the indicator fura-2. Spontaneous rhythmic activity in
terms of slow oscillations from a basal level was observed at 3 mM gl
ucose. Like in the insulin-secreting beta-cells the generation of [Ca2
+](i) oscillations in the alpha-cells was affected by the activity of
the Na/K pump. Blocking the pump with ouabain resulted in an initial r
ise of [Ca2+](i) followed by gradual return to the basal level. The os
cillations were transformed into sustained elevation of [Ca2+](i) by 1
0 mM L-glycine, which is cotransported with Na+. A similar but less pr
onounced effect was obtained when Na+ was cotransported with 10 mM of
the nonmetabolizable amino acid alpha-amino-isobutyric acid. L-glycine
induced sustained increase of [Ca2+](i) also when the oscillatory act
ivity was suppressed by exposing the alpha-cells to 20 mM glucose in t
he presence of insulin. The observation that carbachol induces a [Ca2](i) response in isolated alpha-cells calls for reconsideration of cur
rent ideas that muscarinic stimulation of glucagon release is an indir
ect effect mediated by adjacent beta-cells.