Histamine-induced Ca2+ entry precedes Ca2+ mobilization in bovine adrenal chromaffin cells
- 1 December 1994
- journal article
- Published by Portland Press Ltd. in Biochemical Journal
- Vol. 304 (2), 469-476
- https://doi.org/10.1042/bj3040469
Abstract
The relationship between histamine-induced Ca2+ mobilization and Ca2+ entry in bovine adrenal chromaffin cells has been investigated. Stopped-flow fluorimetry of fura-2-loaded chromaffin cell populations revealed that 10 microM histamine promoted entry of Ca2+ or Mn2+ without measurable delay (< or = 20 ms), through a pathway that was insensitive to the dihydropyridine antagonist nifedipine. In the absence of extracellular Ca2+, or in the presence of 100 microM La3+, a blocker of receptor-mediated Ca2+ entry, 10 microM histamine triggered an elevation in intracellular calcium concentration ([Ca2+]i), but only after a delay of approx. 200 ms, which presumably represented the time required to mobilize intracellular Ca2+. These data suggested that histamine-induced bivalent-cation entry precedes extensive Ca2+ mobilization in chromaffin cells. In order to confirm that histamine can promote Ca2+ entry largely independently of mobilizing intracellular Ca2+, the ability of histamine to promote Ca2+ entry into cells whose intracellular Ca2+ store had been largely depleted was assessed. Fura-2-loaded chromaffin cells were treated with 10 microM ryanodine together with 40 mM caffeine, to deplete the hormone-sensitive Ca2+ store. This resulted in an approx. 95% inhibition of histamine-induced Ca2+ release. Under these conditions, histamine was still able to promote an entry of Ca2+ that was essentially indistinguishable from that promoted in control cells. In single cells, introduction of heparin (100 mg/ml), but not de-N-sulphated heparin (100 mg/ml), abolished the histamine-induced rise in [Ca2+]i. All these data suggest that histamine can induce G-protein- or inositol phosphate-dependent rapid (< or = 20 ms) Ca2+ entry without an extensive intracellular mobilization response in chromaffin cells, which points to activation of an entry mechanism distinct from the Ca(2+)-release-activated Ca2+ channel found in non-excitable cells.Keywords
This publication has 73 references indexed in Scilit:
- Depletion of InsP3 stores activates a Ca2+ and K+ current by means of a phosphatase and a diffusible messengerNature, 1993
- Localization of inositol 1,4,5-trisphosphate receptor-like protein in plasmalemmal caveolae.The Journal of cell biology, 1992
- Variety of Ca2+-permeable channels in human carcinoma A431 cellsThe Journal of Membrane Biology, 1991
- Control of exocytosis in adrenal chromaffin cellsBiochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, 1991
- Caffeine‐Sensitive Calcium Stores in Bovine Adrenal Chromaffin CellsJournal of Neurochemistry, 1991
- Inositol 1,4,5‐trisphosphate activates two types of Ca2+‐permeable channels in human carcinoma cellsFEBS Letters, 1990
- The caffeine‐sensitive Ca2+ store in bovine adrenal chromaffin cells; an examination of its role in triggering secretion and Ca2+ homeostasisFEBS Letters, 1990
- ‘Quanta’ Ca2+ release and the control of Ca2+ entry by inositol phosphates ‐ a possible mechanismFEBS Letters, 1990
- The effect of heparin on the inositol 1,4,5‐trisphosphate receptor in rat liver microsomes Dependence on sulphate content and chain lengthFEBS Letters, 1989
- Agonists stimulate divalent cation channels in the plasma membrane of human plateletsFEBS Letters, 1985