Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Livett, Bruce G.; Marley, Philip D.

doi:10.1111/j.1476-5381.1986.tb10264.x

Cited by 67 publications

(37 citation statements)

References 36 publications

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“…The response to histamine was also partially reduced by the H -antagonist, mepyramine, at 1 m (Figure 2a), a concentration that fully antagonized the H,-receptor effects on catecholamine release and inositol phosphate production in these cells (Livett & Marley, 1986;Wan et al, 1989a). A combination of both mepyramine and cimetidine each at 1 AM, however, completely blocked the cyclic AMP response to histamine.…”

Section: Data Presentation and Statistical Analysismentioning

confidence: 91%

“…In contrast, several classes of H1 binding site have been found in other tissues, including adrenal cortex (Chang et al, 1979). Hl-receptors increase cytosolic Ca2" in isolated chromaffin cells (Staudermann & Pruss, 1990) and they have been known for over 70 years to induce catecholamine secretion (Elliott, 1912;Szczygielski, 1932; see Livett & Marley, 1986). This secretory action is fully dependent on extracellular Ca2" (Poisner & Douglas, 1966;Livett & Marley, 1986;Noble et al, 1988).…”

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

“…Hl-receptors increase cytosolic Ca2" in isolated chromaffin cells (Staudermann & Pruss, 1990) and they have been known for over 70 years to induce catecholamine secretion (Elliott, 1912;Szczygielski, 1932; see Livett & Marley, 1986). This secretory action is fully dependent on extracellular Ca2" (Poisner & Douglas, 1966;Livett & Marley, 1986;Noble et al, 1988). In addition, the H1-receptors are coupled to increased formation of inositol phosphates (Noble et al, 1986;Plevin & Boarder, 1988;Wan et al, 1989a;Staudermann & Pruss, 1990;Bunn et al, 1990) (Rogers et al, 1975;Palacios et al, ie adrenal 1978;Hill et al, 1981), while the cyclic AMP response to histracallulof tamine in homogenates of these tissues was mediated excluhe 2.2mM sively by H2-receptors (Hegstrand et al, 1976;Green et al, timulation 1977).…”

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

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Histamine‐induced increases in cyclic AMP levels in bovine adrenal medullary cells

Marley¹,

Thomson

Jachno

et al. 1991

British J Pharmacology

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1 The effect of histamine on cellular cyclic AMP levels in cultured bovine adrenal medullary cells has been studied.2 Histamine (0.3-30 UM) increased cyclic AMP levels transiently, with a maximal response after 5 min, a smaller response after 20 min, and no increase seen after 80 or 180 min. The EC50 at 5 min was approximately 2 pm. Histamine had no effect on cyclic AMP release from the cells over 5 min, but increased it after 90 min.3 The cyclic AMP response to 5pM histamine was reduced by 45% by 1pM mepyramine and by almost 30% by 1 ,uM cimetidine, and was abolished by the combination of both antagonists. Cimetidine at 100pMdid not inhibit the response to histamine more than 1 M cimetidine. The H3-receptor antagonist, thioperamide (1 pM), had no effect on the response to histamine. 4 The H1-receptor agonist, 2-thiazolylethylamine (5-100pM) and the H2-receptor agonist, dimaprit (5-100pM), each induced a cyclic AMP response, and gave more-than-additive responses when combined.The H3 agonist (R)a-methylhistamine (100pM) had no effect either on its own or in combination with either the H1 or the H2 agonist. The response to 100pM 2-thiazolylethylamine was unaffected by cimetidine (100puM).5 The cyclic AMP responses to 5puM histamine, 100pM thiazolylethylamine and 100pM dimaprit were each weakly enhanced in the presence of 1 mm 3-isobutyl-1-methylxanthine. The response to dimaprit was enhanced more than 10 fold in the presence of 0.3 uM forskolin, while the responses to histamine and thiazolylethylamine were weakly enhanced. 6 The cyclic AMP response to 5,M histamine was partially reduced in the absence of extracellular Ca2 and the residual response was fully antagonized by 1 UM cimetidine and was unaffected by 1 pM mepyramine. In the absence of Ca2 , the cyclic AMP response to 100pM thiazolylethylamine was abolished, while that to 100puM dimaprit was unaffected.7 Reincubation of 5.uM histamine solutions with a second set of chromaffin cells, following prior incubation with another set of cells, induced a cyclic AMP response in the fresh cells. This response was reduced by a combination of mepyramine and cimetidine to the same degree as the response to fresh 5,M histamine solutions. 8 The results indicate that histamine increases cellular cyclic AMP levels in bovine chromaffin cells by three mechanisms: by acting on H1 receptors, by acting on H2 receptors, and by an interaction between H, and H2 receptors. The H1 response does not require concomitant activation of H2 receptors, is fully dependent on extracellular Ca2 +, does not depend on secreted chromaffin cell products, and is not due to reduced cyclic AMP degradation or export. The H2 cyclic AMP response is the first functional response reported for H2 receptors on chromaffin cells, is independent of Ca2 , is not due to reduced cyclic AMP export or degradation, and is likely to be mediated via a direct action through Gs. The role of these different mechanisms in the regulation of cyclic AMP-dependent processes in chromaffin cells by histamine is under investigat...

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Section: Data Presentation and Statistical Analysismentioning

confidence: 91%

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

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Histamine‐induced increases in cyclic AMP levels in bovine adrenal medullary cells

Marley¹,

Thomson

Jachno

et al. 1991

British J Pharmacology

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“…The specificity of NSTX for the nicotinic receptorionophore complex was tested by studying its effects on catecholamine release evoked by K+, which activates voltage-dependent Ca"+ channels directly by depolarizing the chromaffin cell membrane, to bring about exocytosis (Douglas, 1975) and histamine, which evokes release via H,-receptors (Livett & Marley, 1986). NSTX had no effect on either K+-induced or histamine-induced catecholamine release, demonstrating the high specificity of the toxin for the nicotinic response.…”

Section: Discussionmentioning

confidence: 99%

The effects of neosurugatoxin on evoked catecholamine secretion from bovine adrenal chromaffin cells

Bourke¹,

Bunn²,

Marley³

et al. 1988

British J Pharmacology

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1 The effect of neosurugatoxin (NSTX), a toxin from the Japanese ivory mollusc (Babylonia japonica), on the nicotinic response of bovine adrenal chromaffin cells was examined. 2 NSTX inhibited acetylcholine-and nicotine-induced catecholamine secretion from the cultured cells with an ICO against 5 JLM nicotine of 30 nM. 3 This inhibitory effect was reversible and independent of the presence of agonist. 4 NSTX had no effect on the catecholamine release from cultured cells evoked by 50 mM K+, or 1 J1M histamine. 5 NSTX had no effect on the stimulation of phosphatidylinositol metabolism evoked by 100 tiM muscarine.6 These results suggest NSTX may be useful as a nicotinic receptor probe in tissues such as the adrenal and sympathetic ganglia where a-bungarotoxin is ineffective. IntroductionIn studies of receptor-ionophore function in adrenal chromaffin cells, there is currently a need for a better probe for the nicotinic receptor. Hexamethonium is a weak, non-competitive inhibitor of the nicotinic response (Kilpatrick et al., 1981), while x-bungarotoxin binds with high affinity to the chromaffin cells but does not inhibit the nicotinic response (Kumakura et al., 1980;Quik & Trifaro, 1982).Neosurugatoxin (NSTX) is a novel marine toxin recently isolated from the Japanese ivory mollusc, Babyloniajaponica (Kosuge et al., 1981). The structure ofNSTX is shown in Figure 1 , 1974;Hayashi & Yamada 1975; Hayashi et al., 1984).The high affinity of the toxin for ganglionic nicotinic receptors over ganglionic muscarinic receptors has been demonstrated in the isolated superior cervical ganglion of the rat. Extracts of the Japanese ivory mollusc were shown to depress reversibly orthodromic transmission and antagonize the depolarizing action of carbachol on nicotinic receptors, while failing to reduce the depolarizing effects of muscarine (Brown et al., 1976 (Hayashi et al., 1984;Yamada et al., 1985;Rapier et al., 1985).In the present study, the action of NSTX on nicotine-induced catecholamine secretion and muscarine-induced phosphatidyl inositol (PI) metabolism h to allow incorporation of the label.In the standard protocol to test the ability of NSTX to modify muscarine-induced PI metabolism, the dishes were removed from the incubator and the loading medium removed. Each well then received two consecutive 5 min washes at 37°C with incubation buffer of the following composition (mM): NaCI 149, KCl 2.6, K2HPO4 2.15, KH2PO4 0.85, MgSO4 1.18, LiCI 5, glucose 10, pH 7.4. PI metabolism was then stimulated for 30 min at 37'C by 100 pM muscarine in the same incubation buffer. The effects of NSTX and atropine were determined by including the drug in both the second wash and the stimulation period. The incubation was terminated by replacing the buffer with 1 ml ice cold 15% trichloroacetic acid (TCA) and extracting the cells for I h. This TCA was collected into glass tubes, and the cells were rinsed with a further 0.5 ml of TCA which was collected after 5 min.The extraction and analysis of inositol phosphates was performed using a mo...

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“…These channels are regulating the nicotinic and muscarinic secretory response of cat and bovine chromaffin cells [90][91][92]. While ER Ca 2+ release by histamine causes a mild and transient catecholamine release response [93], a more sustained application causes a longer effect [93][94][95]. This greater effect could be explained by the fact histamine-elicited [Ca 2+ ] c elevations has two components: an initial transient phase due to ER Ca 2+ release and a late more sustained phase due to Ca 2+ entry [30,83,96,97].…”

Section: Endoplasmic Reticulummentioning

confidence: 99%

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

et al. 2012

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a b s t r a c tfluxes between the different cell compartments support the proposal that the chromaffin cell has developed functional calcium tetrads formed by calcium channels, cytosolic calcium buffers, the endoplasmic reticulum, and mitochondria nearby the exocytotic plasmalemmal sites. These tetrads shape the Ca 2+ transients occurring during cell activation to regulate early and late steps of exocytosis, and the ensuing endocytotic responses. The different patterns of catecholamine secretion in response to stress may thus depend on such local [Ca 2+ ] c transients occurring at different cell compartments, and generated by redistribution and release of Ca 2+ by cytoplasmic organelles. In this manner, the calcium tetrads serve to couple the variable energy demands due to exo-endocytotic activities with energy production and protein synthesis.

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Effects of opioid peptides and morphine on histamine‐induced catecholamine secretion from cultured, bovine adrenal chromaffin cells

Cited by 67 publications

References 36 publications

Histamine‐induced increases in cyclic AMP levels in bovine adrenal medullary cells

Histamine‐induced increases in cyclic AMP levels in bovine adrenal medullary cells

The effects of neosurugatoxin on evoked catecholamine secretion from bovine adrenal chromaffin cells

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

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