Studies on Cyclic Nucleotides in the Adrenal Gland V. Adenylate Cyclase in the Adrenal Medulla

Shima, Sumio; Kawashima, Yoshiko; Hirai, Masanao; Kouyama, Hiroshi

doi:10.1254/jjp.26.711

Cited by 7 publications

(8 citation statements)

References 19 publications

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“…In the present study using bovine cultured chromaffin cells, we found a reproducible cellular cyclic AMP response to nicotine, DMPP and acetylcholine, although as noted by others (Tsujimoto et al, 1980;Morita et al, 1987), this reponse was transient: at times longer than Shima et al (1976) found they needed periods longer than 20 min before they saw any cyclic AMP response. However, they used slices of bovine adrenal medulla, which may only allow slow penetration of agonists into the tissue.…”

Section: Discussionsupporting

confidence: 75%

“…Cholinoceptor-mediated cyclic AMP responses in adrenal medullary cells Previous studies have found conflicting evidence on the ability of cholinoceptors to increase cyclic AMP levels in chromaffin cells. A number of authors found that carbachol or acetylcholine had no effect on adenylate cyclase activity in membranes prepared from bovine adrenal medulla (Serck-Hanssen 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: 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). Furthermore, cholinoceptor cyclic AMP responses have also been reported in rat, cat and dog adrenal medulla (Guidotti & Costa, 1973;Jaanus & Rubin, 1974;Shima et al, 1978;Tsujimoto et al, 1980).…”

Section: Discussionmentioning

confidence: 98%

“…Cholinergic stimulation is known to increase cytosolic Ca2" levels, diacylglycerol formation and cyclic AMP levels in chromaffin cells (Shima et al, 1976;Eiden et al, 1984;TerBush & Holz, 1986;Morita et al, 1987;TerBush et al, 1988;Wilson, 1988). Several kinases activated by these second messengers may therefore play a role in mediating cholinergic activation of tyrosine hydroxylase.…”

Section: Therein)mentioning

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: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Section: Therein)mentioning

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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“…Although histamine has been shown previously to induce CA release from bovine adrenal medulla (Schneider, 1969;Shima et al, 1976) (Figure 4b). Histamine when administered intravenously to anaesthetized animals has been reported to release Ad selectively from the intact adrenal gland of the cat (StaszewskaBarczak & Vane, 1965) the dog (Schaepdryver, 1959;Narita, 1971), and the rat (Z. Khalil, Marley & Livettunpublished observations).…”

Section: Discussionmentioning

confidence: 73%

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

Livett

Marley

1986

British J Pharmacology

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IThe effect of opioid peptides and morphine on histamine-induced catecholamine secretion has been studied in monolayer cultures of dispersed, bovine adrenal chromaffin cells. 2 Histamine-induced a dose-dependent secretion of both adrenaline and noradrenaline with a threshold dose of approximately 5 nM, an EC50 of 150 nM and maximal secretion at 10 AM. 3 Catecholamine secretion induced by I tM histamine was completely dependent on extracellular calcium, was inhibited in a dose-dependent manner by mepyramine (I nM-l M), and was unaffected by cimetidine (10 M) and hexamethonium (0.1 mM). 4 Dynorphin-1-13 (1 nM-20 1M), metorphamide (O.1 nM-10-IM), morphine (I nM-0. mM) and diprenorphine (I nM -0.1 mM) each had no effect on adrenaline or noradrenaline secretion induced by 1 JAM histamine. 5 The characteristics of histamine-induced catecholamine secretion from bovine adrenal chromaffin cells were similar to those reported previously for cat and rat adrenal medulla being calcium-dependent and mediated by HI histamine-receptors. The results with opioid peptides and morphine suggest that endogenous adrenal opioid peptides do not act on the opioid binding sites found on adrenal medullary chromaffin cells to modify their secretory response to histamine.

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