ResearchHistamine causes Ca2+ entry via both a storemoperated and a store-independent pathway in bovine adrenal chromaffin cells
References (24)
Ionic mechanisms involved in the secretory effects of histamine in the rat adrenal medulla
Eur J Pharmacol
(1993)A model for receptor-regulated calcium entry
Cell Calcium
(1986)Capacitative calcium entry revisited
Cell Calcium
(1990)- et al.
Depleted internal storeactivated Call entry can trigger neurotransmitter release in bovine chromaffin cells
Neurosci Lett
(1996) - et al.
Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool, and not an inositol phosphate, regulates calcium fluxes at the plasma membrane
J Biol Chem
(1989) - et al.
Spontaneous Ca2+ spiking in a vascular smooth muscle cell line is independent of the release of intracellular Ca2+ stores
J Biol Chem
(1993) - et al.
A new generation of Ca2+ indicators with greatly improved fluorescence properties
J Biol Chem
(1985) - et al.
Thapsigargin, a high affinity and global inhibitor of intracellular Ca2+ transport ATPases
Arch Biochem Biophys
(1992) - et al.
Lanthanum can be transported by the sodium-calcium exchange pathway and directly triggers catecholamine release from bovine chromaffin cells
Cell Calcium
(1994) - et al.
Dissociation of Call entry and Call mobilization responses to angiotensin II in bovine adrenal chromaffin cells
J Biol Chem
(1989)
Characterization and Call requirement of histamine-induced catecholamine secretion in cultured bovine chromaffin cells
J Neurochem
Characterization of histamine-induced catecholamine secretion from bovine adrenal medullary chromaffin cells
J Neurochem
Cited by (34)
Cytosolic organelles shape calcium signals and exo-endocytotic responses of chromaffin cells
2012, Cell CalciumCitation Excerpt :While ER Ca2+ release by histamine causes a mild and transient catecholamine release response [93], a more sustained application causes a longer effect [93–95]. This greater effect could be explained by the fact histamine-elicited [Ca2+]c elevations has two components: an initial transient phase due to ER Ca2+ release and a late more sustained phase due to Ca2+ entry [30,83,96,97]. The second component has been associated to inhibition of an M-current by sustained histamine application, leading to cell depolarisation, discharge of action potentials and opening of VDCCs in bovine chromaffin cells [98], although stimulation of SOCCs by ER emptying could also contribute to this effect (see Section 2.2).
Stimulation of histamine H<inf>2</inf> receptors activates TRPC3 channels through both phospholipase C and phospholipase D
2009, European Journal of PharmacologyMechanisms in histamine-mediated secretion from adrenal chromaffin cells
2003, Pharmacology and TherapeuticsCitation Excerpt :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).
Mechanism underlying histamine-induced intracellular Ca<sup>2+</sup> movement in PC3 human prostate cancer cells
2001, Pharmacological ResearchThe orexin OX<inf>1</inf> receptor activates a novel CA<sup>2+</sup> influx pathway necessary for coupling to phospholipase C
2000, Journal of Biological Chemistry