Elsevier

Cell Calcium

Volume 23, Issue 6, June 1998, Pages 379-386
Cell Calcium

Research
Histamine causes Ca2+ entry via both a storemoperated and a store-independent pathway in bovine adrenal chromaffin cells

https://doi.org/10.1016/S0143-4160(98)90094-XGet rights and content

Abstract

The characteristics and properties of the increase in cytosolic [Ca2+] that occurs in bovine adrenal medullary chromaffin cells on exposure to histamine have been investigated. Specifically, these experiments were conducted to determine how much external Ca2+ enters the cell through a (capacitative) Ca2+ entry pathway activated as a consequence of intracellular Ca2+ store mobilization, relative to that which enters independently of store depletion via other channels activated by histamine. In Fura-2 loaded cells continued exposure to histamine (10 μM) caused a rapid but transient increase in cytosolic [Ca2+] followed by a lower plateau that was sustained as long as external Ca2+ was present. In the absence of external Ca2+ only the initial brief transient was observed. In cells previously treated with thapsigargin (100 nM) in Ca2+-free medium to deplete the internal Ca2+ stores, histamine caused no increase in cytosolic [Ca2+] when external Ca2+ was absent. Re-introduction of external Ca2+ to thapsigargin-treated store-depleted cells caused a sustained increase in cytosolic [Ca2+] that was further increased (P < 0.0002) upon exposure to histamine. The histamine-evoked increase was prevented by the H1-receptor antagonist, mepyramine (2 μM). A comparison was made between store-dependent Ca2+ entry consequent upon store mobilization with histamine in Ca2+-free medium and plateau phase Ca2+ entry resulting from stimulation with histamine in Ca2+-containing medium. The latter was found to be approximately 3 times greater in magnitude than the former (P ⪡ 0.0001) at the same concentration of histamine (10 μM). It is concluded that histamine causes Ca2+ entry not only via a capacitative entry pathway secondary to internal store mobilization, but also causes substantial Ca2+ entry through other pathways.

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      During histamine stimulation of chromaffin cells, the [Ca2+]i increases, as determined by using fluorescent Ca2+ indicators. The response is mediated by H1 receptors, being blocked by mepyramine, pyrilamine, or cinnarizine, but not cimetidine (Stauderman & Pruss, 1990; Goh & Kurosawa, 1991; Tanaka et al., 1998; Zerbes et al., 1998; Bödding, 2000). The Ca2+ response is much larger in adrenaline chromaffin cells than in noradrenaline cells (Nunez et al., 1995), presumably reflecting their higher H1 receptor density and larger inositol phosphate response to histamine (Choi et al., 1993).

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