Adenosine Receptors Activate Adenylate Cyclase and Enhance Secretion from Bovine Adrenal Chromaffin Cells in the Presence of Forskolin

Chern, Yijuang; Kim, Kyong‐Tai; Slakey, Linda L.; Westhead, Edward W.

doi:10.1111/j.1471-4159.1988.tb03034.x

Cited by 51 publications

(49 citation statements)

References 24 publications

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“…The phenomenon of evoked cyclic AMP release was noted over 25 years ago by Davoren & Sutherland (1963) and has been reported from rat, cat and dog adrenal glands and from bovine chromaffin cells (Jaanus & Rubin, 1974;Shima et al, 1978;Tsujimoto et al, 1980;Morita et al, 1985;Chern et al, 1988). Whether agonist-induced increases in cyclic AMP export from cells is simply a passive event secondary to the increase in cellular levels or due to a more active regulatory mechanism is not known.…”

Section: Discussionmentioning

confidence: 98%

“…A number of authors found that carbachol or acetylcholine had no effect on adenylate cyclase activity in membranes prepared from bovine adrenal medulla (SerckHanssen et al, 1972;Hurko et al, 1974;Boonyaviroj & Gutman, 1977) while others found no effect of carbachol, acetylcholine, nicotine or DMPP on cyclic AMP levels in slices or isolated cells from this tissue (Shima et al, 1976;Niggli et al, 1984;Chern et al, 1988;Marriott et al, 1988). In contrast, several reports have recorded robust cyclic AMP responses to cholinoceptor agonists in slices of bovine adrenal medulla or in cultured bovine chromaffin cells (Shima et al, 1976;Eiden et al, 1984;Morita et al, 1987;Wilson, 1988).…”

Section: Discussionmentioning

confidence: 99%

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Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Anderson

Robinson

Marley

1992

British J Pharmacology

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1 The regulation of adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels by cholinoceptors has been studied in cultured bovine adrenal medullary cells.2 Acetylcholine (100 JAM), nicotine (10 JAM) and dimethylphenylpiperazinium (20 JAM) each increased cellular cyclic AMP levels 2 to 4 fold over 5 min in the absence of phosphodiesterase inhibitors. The muscarinic agonist acetyl-p-methylcholine (100 JAM) had no effect either on its own or on the response to nicotine. The responses to acetylcholine and nicotine were unaffected by atropine (I JAM) but were abolished by mecamylamine (5 JAM).3 Cellular cyclic AMP increased transiently during continuous exposure to nicotine (1-20 JAM), with the largest response seen after 5 min, a smaller response after 20 min, and no change in cyclic AMP levels seen after 90 or 180 min. The maximal response after 5 min stimulation was seen with 5-10 IJM nicotine and the EC50 was about 2 JAM. In contrast, extracellular cyclic AMP levels did not change after 5 or 20 min stimulation with nicotine, but increased slightly after 90 min and further after 180 min. 4 The cellular cyclic AMP response to nicotine (1O JM) was unchanged or weakly enhanced in the presence of the unselective phosphodiesterase inhibitor, isobutylmethylxanthine, and was unchanged in the presence of rolipram. Nicotine did not interact synergistically with low concentrations of forskolin. The response was however completely abolished in the absence of extracellular Ca2 .5 The nicotinic cyclic AMP response was almost abolished by sphingosine (30 JAM), which did not inhibit the cyclic AMP response to phorbol-12,13-dibutyrate (PDB). The nicotinic response was reduced by 55% by the calmodulin antagonist W7 at 3 JAM, and by >90% at 10 JAM W7. At these concentrations, W7 had no effect on the cyclic AMP response to 100 nM PDB. The nicotinic response was also selectively abolished by another calmodulin antagonist, trifluoperazine (10JLM). 6 The results indicate that nicotinic cholinoceptors can increase cyclic AMP production in chromaffin cells by a mechanism that does not directly involve Gs, that is dependent on extracellular Ca2" and that is sensitive to the calmodulin antagonists W7 and trifluoperazine. We propose that a Ca2+/calmodulinsensitive adenylate cyclase may mediate the nicotinic cyclic AMP response in bovine chromaffin cells.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Anderson

Robinson

Marley

1992

British J Pharmacology

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“…In these conditions ATP, ADP, AMP or adenosine concentrations resulting from diadenosine phosphate degradation must be far below the pM range. Since the Kd values for ATP and adenosine at purinoceptors (Reilly & Burnstock, 1987) and the known effects of adenosine on CA release (Chern et al, 1988) are produced at concentrations in the order of 100pM, an action through these degradation products is probably precluded.…”

Section: Discussionmentioning

confidence: 99%

“…ATP, adenosine diphosphate (ADP) and adenosine inhibit acetylcholine-evoked CA release, probably by prior conversion to adenosine (Chern et al, 1987). In contrast, adenosine can enhance, in a quite complex manner, forskolinmediated secretion (Chern et al, 1988). Chromaffin cells present a single class of high affinity adenosine transporters of the neural type Torres et al, 1986;1988).…”

Section: Introductionmentioning

confidence: 99%

Effect of diadenosine polyphosphates on catecholamine secretion from isolated chromaffin cells

Castro

Torres

Miras‐Portugal

et al. 1990

British J Pharmacology

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1 The action of several diadenosine polyphosphates (AP3A, AP4A and AP5A) on basal, and on nicotineand high K+-evoked, catecholamine (CA) release has been investigated. Each of the three diadenosine polyphosphates weakly but significantly increased basal CA secretion. This enhancement represented about 10% of the response evoked by 2 J1M nicotine. 2 The evoked secretory response to diadenosine polyphosphates had an absolute requirement for extracellular Ca2".3 In contrast, these compounds had an inhibitory action on nicotine-evoked release. This response was concentration-dependent, EC50 values being 3.2 + 0.4OAM, 4.0 + 1.6./M and 19.3 + 4.0/AM for AP A AP4A, and AP5A, respectively. The lower the concentration of nicotine used to evoke secretion, the higher the inhibitory power of these compounds.4 The CA secretion evoked by K+-rich solutions was further enhanced by AP3A and APA, whereas AP4A inhibited it. The possible physiological role of these dual actions is discussed.

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“…ATP is also released from the adrenal capsule and zona glomerulosa region of the gland [23]. Functional studies have shown that ATP can facilitate [12,25] and inhibit [11] catecholamine secretion from adrenal chroma n cells. ATP can also stimulate steroidogenesis from adrenal cortical cells [23,24,27,30].…”

Section: Introductionmentioning

confidence: 99%

Age‐related changes in the localization of P2X (nucleotide) receptors in the rat adrenal gland

Afework¹,

Burnstock

2000

Intl J of Devlp Neuroscience

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Observation of the changes in the occurrence and distribution of nucleotide (P2X) receptors in the adrenal gland during development and ageing, and correlation with the changes in adrenal status at similar stages may give morphological insights into the functions of purine nucleotides in the gland. Age-related changes in the localization of all seven subtypes of the P2X receptor in the adrenal gland of rat were therefore investigated immunohistochemically. In the adrenal glands of prenatal rats, immunoreactivity to P2X receptor subtypes was not observed. In glands of the postnatal rat at the developmental stages studied, only immunoreactivity for the P2X 5 receptor subtype was observed. A small number of faintly P2X 5 -immunoreactive chroma n cells were found in the adrenal glands of 1-day-old rats; the frequency of localization and intensity of staining of immunoreactive cells had increased by day 4 and was further increased at day 7. P2X 5 immunoreactivity was not observed in the adrenal glands from 14-and 21-day-old rats. At 8 weeks of age, immunoreactivity with a speci®c distribution for each of the seven receptor subtypes was observed. Except for the P2X 4 receptor, adrenal glands at 24 months showed a similar pattern of immunoreactivity for the receptor subtypes as that observed at 8 weeks. Immunoreactivity for P2X 4 was ®rst observed in the adrenal cortical cells of the zona reticularis at 8 weeks, but was absent in 24-month-old rats. However, several P2X 4 -immunoreactive chroma n cells appeared at 24 months. Such immunoreactive cells were not seen in rats of any of the other ages studied. It was concluded that the greater expression of P2X 5 receptor at an early developmental stage and of P2X 4 in ageing might re¯ect functional roles for purines in cellular proliferation and/or di erentiation, and in cellular degeneration, respectively, in adrenal glands of rat. 7

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Adenosine Receptors Activate Adenylate Cyclase and Enhance Secretion from Bovine Adrenal Chromaffin Cells in the Presence of Forskolin

Cited by 51 publications

References 24 publications

Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Cholinoceptor regulation of cyclic AMP levels in bovine adrenal medullary cells

Effect of diadenosine polyphosphates on catecholamine secretion from isolated chromaffin cells

Age‐related changes in the localization of P2X (nucleotide) receptors in the rat adrenal gland

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