Dihydropyridine-sensitive and -insensitive voltage-operated calcium channels participate in the control of glucose-induced insulin release from human pancreatic β cells

A. M. Davalli, E. Biancardi, A. Pollo, C. Socci, A. E. Pontiroli, G. Pozza, F. Clementi, E. Sher, E. Carbone

Research output: Contribution to journalArticle

Abstract

Calcium ion entry through voltage-operated calcium channels is a crucial step in the coupling of β cell depolarization with insulin secretion. Various calcium channel subtypes have been shown to be coexpressed in single neurons and endocrine cells. Using the patch-clamp technique, we investigated the biophysical and pharmacological properties of calcium channels in freshly dispersed human pancreatic β cells. Both low and high voltage activated currents were expressed, the two current types being easily distinguishable on the basis of biophysical criteria. The high voltage activated currents were not homogeneous: one component was affected by the dihydropyridine antagonist nitrendipine and the agonist Bay-K-8644; the other was insensitive to both dihydropyridines and ω-conotoxin GVIA. In line with this pharmacology, nitrendipine reduced and Bay-K-8644 increased glucose-induced insulin secretion from perifused human islets, whereas ω-conotoxin GVIA had no effect. However, about 20% of the glucose-induced insulin release was found to be resistant to high nitrendipine concentrations. These data show that human pancreatic β cells express heterogeneous voltage-operated calcium channels, only one of which is dihydropyridine-sensitive (L type). The L type channels are clearly involved in the control of insulin secretion, but our data suggest that dihydropyridine- and ω-conotoxin GVIA-insensitive channels may also play a role in the stimulus-secretion coupling of human β cells.

Original languageEnglish
Pages (from-to)195-203
Number of pages9
JournalJournal of Endocrinology
Volume150
Issue number2
Publication statusPublished - Aug 1996

ASJC Scopus subject areas

  • Endocrinology

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