Effects of theophylline and propranolol on acetylcholine-induced release of adrenal medullary catecholamines

Serck‐Hanssen, Guldborg

doi:10.1016/0006-2952(74)90552-8

Cited by 32 publications

(10 citation statements)

References 18 publications

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“…In this context the controls with isoprenaline seemed important in that postjunctional a*-adrenoceptors in some locations have been reported to inhibit end-organ activity (see Langer 19811, particularly when it is mediated via the adenylate cyclase system, which is the case for amylase secretion from salivary glands (Butcher et dine reduced it to the low level otherwise seen only after B-adrenoceptor block (Gjorstrup 1979 a ) , suggesting that possibly the chromafin cells of the adrenal medulla of the rabbit are endowed with prejunctional a-adrenoceptors. The present evidence for a prejunctional a-adrenoceptor mediated control of catecholamine release from the rabbit adrenals is circumstantial, but is in accordance with earlier observations (Gutman & Bonnyaviro 1974, Serck-Hanssen 1974, Starke et al 1974.…”

Section: Discussionsupporting

confidence: 92%

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Gjörstrup

1984

Acta Physiologica Scandinavica

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In rabbits under urethane anaesthesia parotid secretion of fluid and amylase in response to electrical stimulation of the sympathetic and parasympathetic nerves was measured before and after injections of various agents acting on alpha-adrenoceptors. Amylase secretion in response to sympathetic nerve stimulation at 0.5 and 1 Hz was markedly reduced by clonidine, 0.5-30 micrograms/kg, in a dose related manner. The effect was not due to an altered responsiveness of the gland, since isoprenaline still caused a large release of amylase. Phenylephrine, 10 micrograms/kg, and prazosine, 300 micrograms/kg, had no effect on the sympathetically evoked amylase secretion. Yohimbine in a dose of 0.5 mg/kg increased the amylase output in response to sympathetic nerve stimulation at 0.5 Hz by 70%, while the response at 1 Hz, which is close to maximum for the gland, was not significantly increased. The fluid and amylase secretion produced by parasympathetic nerve stimulation at 1.5, 5.0 and 10 Hz remained unchanged after clonidine, 1.0-30 micrograms/kg, or yohimbine 0.5 mg/kg. In rabbits provided with chronic parotid fistulae fluid and amylase secretion were studied after injections of clonidine, 30 micrograms/kg, and yohimbine, 1 mg/kg. In the conscious animal clonidine reduced not only amylase but also fluid secretion, by around 50 and 30%, respectively, indicating an effect on the activity in both the sympathetic and parasympathetic secretory nerves. Yohimbine increased the output of amylase during feeding, seen as an increased mean output of amylase due to an increased concentration of amylase in the saliva, while fluid secretion remained unchanged. The various experiments suggest that amylase secretion in response to sympathetic activation may be influenced by prejunctional control of transmitter release via alpha-2-adrenoceptors, and that this control may be of physiological significance. Parasympathetically evoked secretion does not seem to be under the influence of a similar control.

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Section: Discussionsupporting

confidence: 92%

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Gjörstrup

1984

Acta Physiologica Scandinavica

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“…In others, it enhanced the nicotinic secretory response or had no effect (Adams & Boarder, 1987;Higgins & Berg, 1988;Morita et al, 1987a,b). Similar contradictory data have been obtained with other drugs that affect cellular adenosine 3': 5'-cyclic monophosphate (cyclic AMP) levels, such as phosphodiesterase inhibitors, or that mimic the actions of cyclic AMP, such as the permeant analogues 8-bromo-and dibutyryl-cyclic AMP (Adams & Boarder, 1987;Marriott et al, 1988;Morita et al, 1985;Tsujimoto et al, 1986;Serck-Hanssen, 1974). The cause of the discrepancies between these studies remains unclear but may include different concentrations or timecourses of cyclic AMP generated in the cells by the procedures used and the different types and concentrations of secretagogues used to evoke catecholamine secretion (see for example Morita et al, 1987a,b;Marriott et al, 1988).…”

Section: Introductionmentioning

confidence: 87%

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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“…In addition, propranolol significantly reduced the enhancement in noradrenaline release elicited by papaverine, even though the granular effect' induced by the phosphodiesterase inhibitor in the presence of propranolol was more pronounced than that observed in the absence of the 3-blocking agent. Yet, this concentration of proprano- Hanssen, 1974) and the guinea-pig vas deferens (Wooten et al, 1973) in the absence of extracellular calcium. It is possible that cyclic AMP may facilitate noradrenaline release by mobilizing intracellular bound calcium and thus increasing the availability of calcium for the stimulation secretion coupling.…”

Section: Discussionmentioning

confidence: 99%

STIMULATION OF PRESYNAPTIC β‐ADRENOCEPTORS ENHANCES [³H]‐N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN

Celuch¹,

Dubocovich²,

Langer³

1978

British J Pharmacology

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1 The effects of isoprenaline, propranolol and phosphodiesterase inhibitors on 3H-transmitter overflow elicited by low frequency nerve stimulation were determined in the isolated perfused spleen of the cat. 2 (-)-Isoprenaline (0.14, 1.4, and 14 nM) produced a concentration-dependent increase in [3H]-transmitter overflow evoked by nerve stimulation at 1 Hz and was more effective at 1 Hz than at 2 hertz. 3 A concentration of propranolol (0.1 im), devoid of neurone blocking activity, blocked this effect of (-)-isoprenaline. These results are compatible with the presence of 0-adrenoceptors in the noradrenergic nerve endings of the cat spleen. 4 (+)-Isoprenaline (140 nM) failed to increase the release of radioactivity induced by nerve stimulation, indicating that the 3-adrenoceptor mediating the facilitation of transmitter release was stereospecific.5 The increase in 3H-transmitter overflow induced by nerve stimulation during exposure to the phosphodiesterase inhibitor, papaverine (27 tiM) was more pronounced than that obtained in the presence of 3-isobutyl-1-methyl xanthine (IBMX) 0.5 mm. The facilitation in transmitter release induced by papaverine was not correlated with the granular effect produced by this drug. 6 In the presence of papaverine, the concentration-effect curve for (-)-isoprenaline on transmitter release was shifted to the left and its maximum was increased. In addition, propranolol significantly reduced the enhancement in noradrenaline release obtained by exposure to papaverine under conditions in which the granular effect produced by the phosphodiesterase inhibitor was even greater than in the absence of the ,-blocker.7 It is concluded that activation of presynaptic 0-adrenoceptors in the perfused cat spleen leads to an enhancement in transmitter release which appears to be linked to an increase in cyclic adenosine 3',5'-monophosphate levels in noradrenergic nerve endings.

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Effects of theophylline and propranolol on acetylcholine-induced release of adrenal medullary catecholamines

Cited by 32 publications

References 18 publications

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

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

STIMULATION OF PRESYNAPTIC β‐ADRENOCEPTORS ENHANCES [³H]‐N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN

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Effects of theophylline and propranolol on acetylcholine-induced release of adrenal medullary catecholamines

Cited by 32 publications

References 18 publications

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

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

STIMULATION OF PRESYNAPTIC β‐ADRENOCEPTORS ENHANCES [3H]‐N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN

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STIMULATION OF PRESYNAPTIC β‐ADRENOCEPTORS ENHANCES [³H]‐N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN