Histamine Evokes Greater Increases in Phosphatidylinositol Metabolism and Catecholamine Secretion in Epinephrine-Containing than in Norepinephrine-Containing Chromaffin Cells (original) (raw)
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Life Sciences, 1997
The effects of histamine on catecholamine secretion from cultured bovine adrenal chromaffin cells were studied in the presence of ouabain, an inhibitor of Na+-K+ ATPase. The purpose of this study was to determine whether Na+, as well as Ca2+, was involved in histamine receptor-mediated catecholamine secretion. Histamine (lo-*-lo-sM)-induced catecholamine secretion was markedly potentiated by addition of ouabain (lo-5M) and was inhibited by a histamine-HI receptor antagonist or incubation in a Ca2+-free medium. Histamine-induced 45Ca2+ influx was also potentiated by addition of ouabain. Ouabain alone or in the presence of histamine increased 22Na+ influx into the cells. In an additional set of experiments, cells were preincubated in the presence or absence of Na+ for 30min (& histamine and ouabain), washed and then catecholamine secretion was measured following exposure to 2.2mM Ca2+ for 15min. Preincubation with histamine alone with or without Na+ had no effect of Ca2+-induced secretion of catecholamine. Preincubation with ouabain alone or with ouabain plus histamine produced a slight stimulation of catecholamine secretion in Na+-free medium and a large stimulation in Na+-containing medium. These results suggested that stimulation of the histamine-HI receptor and inhibition of the Na+ pump both increase intracellular Na+ levels, resulting in increases in Ca2+ influx and catecholamine secretion.
The Journal of physiology, 1987
1. We have studied the mechanism of catecholamine secretion induced by histamine from the adrenal medulla and sympathetic noradrenergic neurones in the rat, and the role of capsaicin-sensitive sensory nerves in this secretion. 2. Histamine at a dose of 1 mg/kg induced adrenaline and noradrenaline secretion by a non-neurogenic mechanism. In contrast, at a dose of 3 mg/kg it induced adrenaline and noradrenaline secretion by both non-neurogenic and neurogenic mechanisms. 3. The adrenaline released in response to histamine at 3 mg/kg was exclusively of adrenal origin whereas the noradrenaline released was of non-adrenal origin (most probably noradrenergic sympathetic nerves). As with its action on the adrenal, histamine induced noradrenaline secretion from these extra-adrenal tissues by both neurogenic and non-neurogenic mechanisms. 4. When adrenaline secretion from the adrenal gland was impaired by adrenal denervation and/or adrenalectomy, the plasma noradrenaline secretion was increas...
Regulation of Norepinephrine Release from Isolated Bovine Irides by Histamine
Neurochemical Research, 2006
In the present study, we investigated the effect of histamine on sympathetic neurotransmission from isolated, superfused bovine irides. We also studied the pharmacology of prejunctional histamine receptors that regulate the release of norepinephrine (NE) from this tissue. The effect of exogenous histamine and various histamine receptor agonists was examined on the release of [ 3 H]-norepinephrine ([ 3 H]NE) triggered by electrical field stimulation using the Superfusion Method. Histamine receptor agonists caused a concentration-dependent inhibition of fieldstimulated [ 3 H]NE overflow with the following rank order of potency: imetit > histamine > R-a-methylhistamine. In all cases, the inhibitory action of histamine receptor agonists was attenuated at high concentrations of these compounds. The histamine receptor antagonists, clobenpropit (H 3-antagonist/H 4-agonist) and thioperamide (H 3-antagonist) blocked the inhibitory response elicited by R-a-methylhistamine and imetit, respectively. Inhibitory effects of R-a-methylhistamine and clonidine were not additive suggesting that prejunctional H 3-and a 2-adrenoceptors coexist at neurotransmitter release sites. We conclude that histamine produces an inhibitory action on sympathetic neurotransmission in the bovine iris, an effect mimicked by selective H 3-receptor agonists and blocked by H 3-antagonists.
Histamine activates phosphorylase and inositol phosphate production in guinea pig hepatocytes
European Journal of Pharmacology: Molecular Pharmacology, 1992
In guinea pig hepatoqtes, histamine increased phosphorylase activity and inositol phosphate production. Similar effects were obtained with Z-(2-aminoethyl)-thiazole, a histamine H, receptor agonist, but not with dimaprit or impromidine, H, receptor agonists. These effects of histamine were dose-dependently inhibited by the H, antihistamines, (+)-chlorpheniramine and mepyraminc fpyrilamine) but not by cimetidine or ranitidine, Hz antagonists. (+I-Chlorpheniramine and mepyraminc had similar potencies (apparent Ki values =; 3 nM) when incubated with the cells for I min (phosphorylase a assays) but the former was 15-20-fold more potent than the latter at longer incubation times (apparent Ki values = 3-4 nM and 45-90 nM, respectively) indicating that mepyraminc is actively metabolized by guinea pig hepatocytes. Histamine increased cytosol calcium approximately Z-fold, an effect also mediated through H, receptors. The actions of histamine were not affected by in vivo ADP-ribosylation by pertussis toxin. Our data clearly indicate that histamine modulates the metabolism of guinea pig hepatocytes via activation of H, receptors. These receptors are coupled to the phosphoinositide turnover-calcium mobilization signalling pathway through a pertussis toxin-insensitive process.
Journal of Neurochemistry, 2002
In this report we investigate the isoforms of protein kinase C (PKC) present in cultured adrenal chromaffin cells with respect to their modulation by treatment with phorbol ester and their possible differential involvement in the regulation of responses to histamine and bradykinin. The presence of individual isoforms of PKC was investigated by using eight isoform specific antisera, as a result of which PKC-a, , and~were identified. To characterize down-regulation of these enzymes, cells were incubated for 6-48 h with 1 1iM phorbol myristate acetate (PMA). PKC-down-regulated more rapidly than PKC-a. At 12 h, PMA pretreatment, for example, PKC-e was maximally down-regulated (23 ±4% of controls), whereas PKC-a was unchanged. PKC-cs showed partial down-regulation by 24 h of PMA pretreatment. PKC-did not down-regulate at any of the times tested. Translocation from cytosol to membrane in response to PMA was also more rapid for PKC-e than for PKC-a. The accumulation of total 3H-inositol (poly) phosphates in response to bradykinin or histamine was essentially abolished by prior treatment with 10-mm PMA treatment (1~tM).However, with 12-h exposure to PMA, the bradykinin response was restored to the level seen with no prior PMA exposure. The histamine response showed no recovery by 12 h of PMA, but showed partial recovery by 24 h of PMA pretreatment. These observations showed that the restoration of the response to bradykinin corresponds to the loss of PKC-,whereas the restoration of the histamine response corresponds to the loss of PKC-a. This picture was confirmed with further studies on cytosolic Ca2~. The results show that chromaffin cells exhibit an unusual pattern of down-regulation of PKC isoforms on prolonged exposure to PMA, and that there is a differential effect of exposure to PMA on the histamine and bradykinin responses, suggesting that different PLC-linked receptors in chromafin cells are differentially regulated by PKC isoforms. Key Words: Chromaffin cells-Protein kinase C isoforms-Bradykinin -Histamine-Feedback.
The physiological role of histamine in the exocrine pancreas
Inflammation Research, 1997
In addition to the autonomic nervous system and gut hormones, the mast cell mediator histamine has also been associated with exocrine pancreatic secretion. This review is concerned with the distribution and the physiological role of histamine in the control of pancreatic juice secretion. Histamine is distributed widely around blood vessels and acinar tissues in the pancreas and it is released in pancreatic juice during secretagogue stimulation. Histamine has a marked secretagogue effect in the exocrine pancreas of several animal species but in many cases the secretory effect is gender-related. The paracrine hormone exerts its secretory response via activation of H 1 and H 2 receptors on pancreatic acinar cells to mobilize potassium ions (K þ ) and cellular calcium (Ca 2þ ) and through elevation of endogenous adenosine 3 0 , 5 0 cyclic monophosphate (cyclic AMP) levels, respectively. A physiological role for H 3 receptors has also been associated with exocrine pancreatic secretion. H 3 receptors are located presynaptically on parasympathetic nerve terminals to control the release of acetylcholine via restriction of Ca 2þ access into nerve terminal through the N-type Ca 2þ channel. Taken together, the results presented in this review strongly support histamine as a potential modulator of exocrine pancreatic function.
Neurohormonal regulation of histamine release from isolated rabbit fundic mucosal cells
Agents and Actions, 1993
Histamine-containing cells isolated from rabbit fundic mucosa were found in a small cell elutriation fraction (cells with diameter about 9-12 gm) enriched in mucus and endocrine cells and containing less than 1% mast cells (F 1 cells). Gastrin (HG-17), pentagastrin and CCK-8 (C-terminal octapeptide of cholecystokinin) dose-dependently stimulated histamine release (EC5 o, respectively, 0.126 + 0.03, 0.92 + 0.15 and 0.211 _+0.025 nM) and somatostatin inhibited this release. PGEt, PGE2 and PGD 2 alone were unable to enhance histamine release even at high concentrations but, when used in combination with gastrin of CCK-8, the release of histamine caused by these peptides was potentiated (about 1.5-to 2-fold). Carbachol also enhanced the liberation of histamine but with a weaker potency and efficacy than the gastrointestinal peptides (ECso: 1.50+0.06 gM). The use of specific muscarinic antagonists for Ml-, U 2-and M3-type receptors led us to conclude that an M 1 receptor might be involved in the muscarinic-induced stimulation of histamine release. Activators of protein kinase C, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1oleyl-2-acetyl-glycerol (OAG) as well as the calcium ionophore, A23187, induced histamine release, whereas agents which increased intracellular cAMP content were devoid of effect. All these results allowed us to conclude that (i) in our cell preparation, histamine could be stored in endocrine cells (ECL cells) as its release appears to be under neurohormonal control, (ii) the muscarinic stimulation probably involves an Ml-type receptor located on these cells, (iii) the phosphoinositide breakdown/protein kinase C activation pathway plays an important role in the intracellular regulation, leading to the liberation of histamine.
Hypothalamic H1 and H2 receptors: A tool to investigate the neuroendocrine role of histamine
Pharmacological Research Communications, 1980
The interaction between sexual o~ adrenal steroids and histamine receptors in rat hypothalamus was studied. The hypothalamic histaminesensitive adenylate cyclase was stimulated by both estradiol and 2-hy-dro~,-estradlol, but no~ by progesterone or methyl-testosterone. Estrogens inhibited the histamine induced stimulation; on the contrary progesterone and methyl-.testosterone were unable to antagonize the histamine stimulating effect. Aldosterone and hydrocortisone also stimulated the hypothalam/c histamine-sensitlve adenylate cyclase. Aldmsterone inhibited the 4-methyl-hlstamine induced st/mulation, on the other hand hydrocortlsone inhibited the 2-(2-pyridyl)ethylamlne induced ed stimulation. Such results see~ to confirm an interaction between se~l or adrenal steroids and histamine receptors. Moreover the hypothalamic H I and H 2 receptors may represent the sites where histamine parteclpates in a feed back mechanism regulating gonadotropin, prolactin and vasopressin secretion.
Cell Biology International, 2014
We have assessed the effect of bradykinin and histamine on the cytosolic free calcium concentration ([Ca 2þ ] i ) of bovine adrenal medulla capillary endothelial cells (BAMCECs). To measure [Ca 2þ ] i changes in BAMCECs the intracellular fluorescent probe, fluo-3 AM, was used. Bradykinin (3 mM) produced a transient monophasic increase in [Ca 2þ ] i , which was depressed by B1650 (0.1 mM), a B2-bradykinin receptor antagonist (D-Arg-[Hyp 3 , Thi 5,8 , D-Phe 7 ]-Bradykinin). Similarly, increase in [Ca 2þ ] i induced by histamine was also depressed by tripolidine (0.1 mM), an H1-histamine receptor antagonist.