Cyclic AMP in the regulation of exocytosis in the rat parotid gland Evidence obtained with cholera toxin

Spearman, Terry N.; Durham, John P.; Butcher, Fred R.

doi:10.1016/0304-4165(83)90196-4

Cited by 13 publications

(7 citation statements)

References 17 publications

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“…A prominent role for cAMP in amylase secretion from parotid glands is well-documented and has been reviewed by Butcher and Putney (1980). In response to 3-adrenergic agonists, such as epinephrine and isoproterenol, parotid glands secrete amylase in vivo (Ikeno et al, 1983) and in vitro (Butcher and Putney, 1980;Spearman et al,1983).…”

Section: Introductionmentioning

confidence: 98%

Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

1985

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The effect ofNaF on the cAMP concentration in and amylase secretion from rat parotid glands in vitro and in vivo was investigated. In vitro, NaF (0.05 to 10 mmol/l) was found to increase significantly amylase secretion and cAMP concentration in parotid gland slices. In vivo, male rats injected intraperitoneally with 15 mg F/kg body weight as NaF had a significantly lower glandular amylase activity and higher plasma amylase activity than did the control rats injected with 0.9% NaCl. Thefluoride concentration both in the parotid gland and plasma was highest at 30 min after injection and decreased with time in the fluoride-injected group. The concentration of the parotid gland cAMP in the fluoride-injected group was significantly higher than that in the control group. On the basis of these results, it is suggested that NaF, both in vitro and in vivo, increases the cAMP concentration, which subsequently stimulates amylase secretion from rat parotid glands.

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Section: Introductionmentioning

confidence: 98%

Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

1985

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“…2 and 3) also suggest that the cyclic AMP level in parotid tissue may not be a major factor responsible for the decreased release of amylase in ISO-treated rats. Spearman et al (11 ) showed that a measurable increase of cyclic AMP in parotid acinar cells is not necessary for the induction of amylase release by (3-adrenergic stimu lation. However, if the amylase release and cyclic AMP accumulation in parotid acinar cells may be regulated by two different (3 adrenoceptor subtypes, 31 and 32 (16), the above mentioned (8) decrease of (3 adrenoceptors might have to be reexamined on each subtype.…”

Section: Animalsmentioning

confidence: 99%

“…When salivation was stimulated by pilocarpine in rats, the degree of increase in the flow rate of parotid saliva and the concentration of amylase in it were lower in ISO-treated rats than in intact animals (6). Although a similar decrease in the flow rate and protein concen tration of parotid saliva of treated rats was observed after an administration of ISO used as a challenge dose, no significant change was found in concentration of electrolytes in the same saliva (7).It is reported that the number and/or affinity of binding sites for i3-adrenergic agonists in the parotid tissue is decreased by the repeated administration of ISO (8, 9) and, on the other hand, that the increase in cyclic AMP in parotid acinar cells by stimu lation of 3-adrenoceptors may not be es sential for ISO-induced amylase release from these cells (10,11). If the effects of i9 adrenergic and muscarinic agonists on parotid amylase secretion were to decrease concomitantly after repeated treatment with ISO (6, 7), the desensitization of i9 adrenoceptors might be considered to be insufficient to explain the mechanism of the decreased response to a challenge dose of ISO.…”

mentioning

confidence: 99%

“…It is reported that the number and/or affinity of binding sites for i3-adrenergic agonists in the parotid tissue is decreased by the repeated administration of ISO (8, 9) and, on the other hand, that the increase in cyclic AMP in parotid acinar cells by stimu lation of 3-adrenoceptors may not be es sential for ISO-induced amylase release from these cells (10,11). If the effects of i9 adrenergic and muscarinic agonists on parotid amylase secretion were to decrease concomitantly after repeated treatment with ISO (6, 7), the desensitization of i9 adrenoceptors might be considered to be insufficient to explain the mechanism of the decreased response to a challenge dose of ISO.…”

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confidence: 99%

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Effects of repeated exposure to isoproterenol in vivo and in vitro on amylase release from rat parotid tissue.

et al. 1984

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Abstract-Effects of repeated exposure to isoproterenol (ISO), in vivo and in vitro, were investigated on amylase release from rat parotid slices responding to secre tagogues. Responses to ISO and dibutyryl cyclic AMP (DBcAMP) were reduced in the tissue from ISO-treated rats (3 mg/kg, 3 times daily for 3 days), but not in the tissue from propranolol plus ISO-treated rats. Administration of inhibitors of protein synthesis with ISO resulted in a protective effect with regard to development of decreased responses to ISO, DBcAMP and carbachol. A decreased response to ISO (10-5 M) was caused by repeated exposure to ISO in vitro and could not be prevented by pretreatment with inhibitors of protein synthesis. Although the basal level of cyclic AMP in parotid tissue was lower in ISO-pretreated rats than in control rats, after incubation with ISO, the level of cyclic AMP did not differ between ISO pretreated and control rats. These results suggest that the decreased response (amylase release) to ISO in the parotid tissue from ISO-pretreated rats may have been due to an impairment of common secretory process(es) involving various secretagogues and that the development of the impairment may be closely con nected to the de novo synthesis of proteins induced by ISO, but not the impairment of the l3-adrenoceptor-adenylate cyclase system.Since it was reported that repeated admin istration of isoproterenol (ISO) in rats caused an enlargement of the salivary glands (1), evidence showing ISO-induced increases of DNA and protein synthesis in these glands has accumulated (2-5). When salivation was stimulated by pilocarpine in rats, the degree of increase in the flow rate of parotid saliva and the concentration of amylase in it were lower in ISO-treated rats than in intact animals (6). Although a similar decrease in the flow rate and protein concen tration of parotid saliva of treated rats was observed after an administration of ISO used as a challenge dose, no significant change was found in concentration of electrolytes in the same saliva (7).It is reported that the number and/or affinity of binding sites for i3-adrenergic agonists in the parotid tissue is decreased by the repeated administration of ISO (8, 9) and, on the other hand, that the increase in cyclic AMP in parotid acinar cells by stimu lation of 3-adrenoceptors may not be es sential for ISO-induced amylase release from these cells (10,11). If the effects of i9 adrenergic and muscarinic agonists on parotid amylase secretion were to decrease concomitantly after repeated treatment with ISO (6, 7), the desensitization of i9 adrenoceptors might be considered to be insufficient to explain the mechanism of the decreased response to a challenge dose of ISO. The present study was undertaken to clarify whether the decreased response to ISO in enlarged parctid glands is mainly due to the impairment of the (9-adrenoceptor adenylate cyclase system. Materials and Methods Animalsand pretreatments: Male Wistar rats weighing 180-200 g were used. These animals were deprived of food 18 hr...

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“…an exogenous agonist. These agonists are used at high, generally maximal or supramaximal concentrations and applied, for prolonged periods of up to 60 min (Butcher, Goldman & Nemerovski, 1975;Spearman, Durham & Butcher, 1982;Yoshimura, Nezu & Chiba, 1982;Hata, Ishida, Kagawa, Kondo, Kondo & Noguchi, 1983). In addition, the changes in cyclic nucleotide content, but not amylase release, have been demonstrated in the presence of a phosphodiesterase inhibitor, theophylline or 3-isobutyl-1-methylxanthine (IBMX) (Butcher, Rudich, Emler & Nemerovski, 1976;Hata et al 1983;Spearman, Durham & Butcher, 1983).…”

Section: Introductionmentioning

confidence: 99%

Beta‐adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3‐isobutyl‐1‐methylxanthine.

Fuller¹,

Gallacher²

1984

The Journal of Physiology

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SUMMARY1. The technique of electrical field stimulation (e.f.s.) was employed in conjunction with selective pharmacological antagonists to specifically investigate the role of endogenous neurotransmitter(s) in the activation off-adrenergic receptor mechanisms in isolated parotid gland segments of the rat.2. The field-stimulus-induced amylase release due tofl-adrenergic receptor activation was characterized as that persisting in the presence of atropine (10-5 M) and phentolamine (10-5 M) and susceptible to blockade by propranolol (5 x 10-6 M), i.e. 3. In the absence of any phosphodiesterase inhibitor the levels of cyclic AMP in the tissues were close to the limit of detection. Field stimulation was however associated with a fourfold increase in cyclic AMP. By comparison isoprenaline (10-5 M) gave rise to a tenfold increase in cyclic AMP.4. The changes in cyclic AMP metabolism, in response to both field stimulation and isoprenaline, were greatly enhanced in the presence ofthe phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). The field-stimulus-induced increase in cyclic AMP was abolished by the 8l1-adrenergic receptor antagonist, metoprolol, but persisted in the presence of the fl2-adrenergic antagonist, H35/25. 5. IBMX was found to have a potent direct effect on amylase release. IBMX (10-3 M) also gave rise to a tenfold increase in cyclic AMP. IBMX is then as effective as 10-5 M-isoprenaline in stimulating both enzyme secretion and cyclic AMP metabolism.6. The secretary response to IBMX was unaffected by fl-adrenergic blockade by propranolol, was independent of extracellular calcium and did not give rise to s6Rb+ efflux.7. Importantly, isoprenaline (10-5 M) failed to evoke any significant increase in amylase release if introduced during sustained superfusion of IBMX, yet it is in such protocols that the greatest changes in cyclic AMP metabolism are seen.* To whom correspondence should be addressed.C. M. FULLER AND D. V. GALLACHER 8. The study clearly demonstrates that the fl-adrenergic-receptor-regulated amylase release in response to nerve stimulation is mediated predominantly, if not exclusively, by the fl1-receptor subtype. It is apparent however that the changes in cyclic AMP measured in the presence of the phosphodiesterase inhibitor, IBMX, do not correlate with enzyme secretion.

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Cyclic AMP in the regulation of exocytosis in the rat parotid gland Evidence obtained with cholera toxin

Cited by 13 publications

References 17 publications

Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

Effect of NaF on Rat Parotid Gland Amylase Activity and cAMP Concentration in vitro and in vivo

Effects of repeated exposure to isoproterenol in vivo and in vitro on amylase release from rat parotid tissue.

Beta‐adrenergic receptor mechanisms in rat parotid glands: activation by nerve stimulation and 3‐isobutyl‐1‐methylxanthine.

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