beta 1- and beta 2-adrenoceptor agonists have different effects on rat parotid acinar cells

Henriksson, Robin

doi:10.1152/ajpgi.1982.242.5.g481

Cited by 20 publications

(26 citation statements)

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“…Judging from the results on the cyclic AMP content, adenylate cyclase activity in the parotid tissue was sub-sensitive after IPR pre-treatment regardless ofthe incubation period. A marked difference between changes in cyclic AMP content and amylase secretion in rat parotid tissue was also reported (Butcher et al 1975;Yoshimura, Nezu & Chiba, 1982;CarlsbS, Danielsson, Henriksson & Idahl, 1982;Henriksson, 1982). Thus the linkage of adenylate cyclase activity with amylase secretion requires further study.…”

Section: Alterations In F-receptors and Secretionmentioning

confidence: 67%

beta‐Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Hata¹,

Ishida²,

Kagawa³

et al. 1983

The Journal of Physiology

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SUMMARY1. Simultaneous studies on the secretary response of amylase and the neurotransmitter receptors ofrat parotid gland, after brieftreatment with agonists, showed selective alteration in /1-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretary response.2. The fl-adrenergic agonist (± )-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration ofan a-adrenergic or cholinergic agonist.3. The stimulatory effects of JPR were studied by pre-treating rat parotid tissues with IPR for 10 min and then incubating the tissue in fresh medium for 10 min.Pre-treatment with 10 ,pM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC60 value of amylase secretion for IPR.4. This treatment also resulted in selective changes in the number and affinity of 8. The alteration in fl-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.

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Section: Alterations In F-receptors and Secretionmentioning

confidence: 67%

beta‐Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Hata¹,

Ishida²,

Kagawa³

et al. 1983

The Journal of Physiology

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“…The latter was performed by using an ocular with 10 x 10 grid mesh and counting 'hits' at the crossings (cross-points). One hundred points per section were counted (Weibel, 1979;Henriksson, 1982). Specimens from both irradiated glands and contralateral controls were fixed and embedded in parallel (Henriksson, 1982;Franzen et al, 1991).…”

Section: Morphological Evaluationsmentioning

confidence: 99%

Increase in mast cells and hyaluronic acid correlates to radiation-induced damage and loss of serous acinar cells in salivary glands: the parotid and submandibular glands differ in radiation sensitivity

Henriksson

Frojd²,

Gustafsson³

et al. 1994

Br J Cancer

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Summary The detailed mechanisms which can explain the inherent radiosensitivity of salivary glands remain to be elucidated. Although DNA is the most plausible critical target for the lethal effects of irradiation, interactions with other constituents, such as cell membrane and neuropeptides, have been suggested to cause important physiological changes. Moreover, mast cells seem to be closely linked to radiation-induced pneumonitis. Therefore, in the present study the effects of fractionated irradiation on salivary glands have been assessed with special regard to the appearance of mast cells and its correlation with damage to gland parenchyma. Sprague-Dawley strain rats were unilaterally irradiated to the head and neck with the salivary glands within the radiation field. Although the detailed mechanisms by which radiation induces damage in biological tissues are not fully understood, it is generally accepted that generation of free radicals is of major importance. DNA is the most likely target for the lethal effects of these irradiation induced free radicals, however it is plausible that other compartments, i.e. non-genetic macromolecules, such as proteins and carbohydrates, can be significantly affected with vital alterations in the functional integrity of the certain biological tissues (Creasy, 1960;Desai et al., 1964;Sutherland et al., 1967;Alper, 1977;El-Mofty et al., 1981;Franzen et al., 1991;1993). In addition, changes caused by external factors and in the surrounding tissues can play an important role in modifying the final detectable and evaluable reaction, which indeed has recently been proposed, e.g. ongoing smoking depressed pneumonitis caused by irradiation in humans (Franzen et al., 1989;Bjermer et al., 1990; as well as in experimental animals . Moreover, sublethal damage following fractionated irradiation seems to cause alterations in cell membrane function and in physiological parameters (Reade & Steidler, 1985; Stephens et al., 1986a,b;Franzen et al., 1991). Most recently, it was also demonstrated that irradiation enhances the expression of important neutopeptides/growth factors, at least in salivary glands (Forsgren et al., 1992;Franzen et al., 1993). Furthermore, parotid acinar cell death following irradiation has been described as an interphase death (Stephens et al., 1986a,b;Franzen et al., 1991).The remarkable sensitivity of salivary gland acinar cells compared with other glands to radiation is a unique radiobiological phenomenon (Shannon et al., 1978;Mira et al., 1982;Abok et al., 1984;Junglee et al., 1986;Franzen et al., 1991). Other well-differentiated gland cells are known to be more or less radioresistant (Rubin & Casarett, 1972). The exact mechanism which explains this sensitivity is not entirely understood. Since mast cells have been proposed to interact in a substantial manner with the development of radiationinduced pneumonitis and pulmonary fibrosis (Franzen et al., 1989;Bjermer et al., 1990; Nilsson et al., 1990a,b; we found it of interest to evaluate the correlation of connecti...

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“…Receptors of the ␤ 2 -subtype are also demonstrable in rat parotid glands, in which the ␤-adrenergic receptor population is primarily of the ␤ 1 -subtype (1,25,27). Although secretory responses of salivary glands to ␤-adrenergic agonists are generally thought to be mediated by receptors of the ␤ 1 -subtype, a number of studies have implicated a role for ␤ 2 -adrenergic receptors in regulation of both salivary secretion and growth (4,24). Whether modification of ␤ 2 -adrenergic receptor content, as we have observed in HSY cells treated with EGF, may in turn modulate salivary gland function remains to be clarified.…”

Section: Discussionmentioning

confidence: 81%

Epidermal growth factor upregulates β-adrenergic receptor signaling in a human salivary cell line

Yeh

Hymer

Sousa

et al. 2003

American Journal of Physiology-Cell Physiology

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epidermal growth factor (EGF) on the ␤-adrenergic receptor-coupled adenylyl cyclase system were studied in a human salivary cell line (HSY). The ␤-adrenergic agonist isoproterenol (10 Ϫ5 M) stimulated adenylyl cyclase activity by ϳ2-fold, and the isoproterenol response was increased 1.8-fold after prolonged (48 h) exposure to EGF (5 ϫ 10 Ϫ10 M). In contrast, enzyme activation via stimulatory prostaglandin receptors and by agents acting on nonreceptor components of the adenylyl cyclase system was not enhanced by EGF. ␤-Adrenergic receptor density, assessed by binding of the ␤-adrenergic receptor antagonist (Ϫ)-[125 I]iodopindolol, was increased threefold after EGF treatment. Competition binding studies with unlabeled antagonists selective for ␤1-and ␤2-adrenergic receptor subtypes indicated that the increase in (Ϫ)-[ 125 I]iodopindolol binding sites induced by EGF reflected an increased number of ␤2-adrenergic receptors. Likewise, Northern blot analysis of RNA from EGF-treated cells revealed selective induction of ␤2-adrenergic receptor mRNA, which was blocked by the RNA synthesis inhibitor actinomycin D. The increase in ␤-adrenergic receptor density produced by EGF was unaltered after phorbol ester-induced downregulation of protein kinase C (PKC). Enhancement of isoproterenol-responsive adenylyl cyclase activity and phosphorylation of mitogen-activated protein kinase (MAPK) by EGF were both blocked by the MAPK pathway inhibitor PD-98059. The results suggest that in HSY cells EGF enhances ␤-adrenergic responsiveness by upregulating ␤2-adrenergic receptor expression at the transcriptional level. Moreover, the stimulatory effect of EGF on ␤2-adrenergic receptor signaling appears to be mediated by the MAPK pathway and independent of PKC activation. adenylyl cyclase; G protein-coupled receptor; signal transduction; mitogen-activated protein kinase; protein kinase C SALIVARY GLAND FUNCTION is tightly regulated by the autonomic nervous system through the actions of neurotransmitters on G protein-coupled receptor signaling pathways (3). In general, cholinergic-muscarinic and ␣-adrenergic receptor agonists induce secretion of salivary fluid and electrolytes via activation of the intracellular calcium ([Ca 2ϩ ] i ) cascade (3). On the other hand, ␤-adrenergic receptor agonists stimulate the secretion of salivary proteins by activation of adenylyl cyclase and the generation of intracellular cAMP (3). Stimulation of the ␤-adrenergic receptor-coupled adenylyl cyclase pathway also causes transcriptional and posttranslational modifications of salivary gland proteins (52). In vivo, the ␤-adrenergic agonist isoproterenol has been demonstrated to induce hypertrophy and hyperplasia of salivary glands (10, 50). In a number of cell types, ␤-adrenergic receptor activation of adenylyl cyclase is modulated by systemic hormones as well as local growth factors and cytokines (21,29,51,54). Whether similar modulation of ␤-adrenergic receptor signaling might play a regulatory role in salivary cell secretion and growth has not been well ch...

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beta 1- and beta 2-adrenoceptor agonists have different effects on rat parotid acinar cells

Cited by 20 publications

References 0 publications

beta‐Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

beta‐Adrenoceptor alterations coupled with secretory response in rat parotid tissue.

Increase in mast cells and hyaluronic acid correlates to radiation-induced damage and loss of serous acinar cells in salivary glands: the parotid and submandibular glands differ in radiation sensitivity

Epidermal growth factor upregulates β-adrenergic receptor signaling in a human salivary cell line

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