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

Hata, Fumiaki; Ishida, Hideyuki; Kagawa, Kimiya; Kondo, Etsuo; Kondo, Shun; Noguchi, Yutaka

doi:10.1113/jphysiol.1983.sp014800

Cited by 38 publications

(16 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rat parotid acinar cells (Fig. 2B), the labeling was especially associated with the apical microvilli, including those situated in the intercellular secretory canaliculi, consistent with previous observations (9). Immunoelectron microscopy also demonstrated that the punctate appearance of the AQP-5 distribution in both glands was due to the clustering of labeling around the microvilli separated by relatively unlabeled nonmicrovillous plasma membrane domains.…”

Section: Subcellular Localization Of Aqp-5 In Salivary Glands By Lighsupporting

confidence: 72%

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Gresz

Kwon

Gong

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

In vitro studies of cultured salivary gland cells and gland slices have indicated that there may be regulated translocation of aquaporin (AQP)-5 between the apical plasma membrane and intracellular compartments of the secretory cells. However, it remains unknown whether AQP-5 in salivary glands is subject to regulated trafficking in vivo. To examine this possibility, we have investigated the subcellular localization of AQP-5 in rat parotid and submandibular glands fixed in vivo under conditions of stimulated or inhibited salivary secretion. Immunofluorescence and immunoelectron microscopy was used to determine the subcellular distribution of AQP-5 in control conditions following the stimulation of secretion with pilocarpine (a muscarinic agonist) or epinephrine (an α-adrenoceptor agonist) or during inhibition of basal secretion with atropine (a muscarinic antagonist) or phentolamine (an α-adrenoceptor antagonist). Under control conditions, >90% of AQP-5 was associated with the apical plasma membrane of acinar and intercalated duct cells, with only rare gold particles associated with intracellular membrane domains. Pilocarpine treatment dramatically increased saliva production but had no discernible effect on AQP-5 distribution. However, the increased salivary secretion was associated with luminal dilation and the appearance of a markedly punctate AQP-5 labeling pattern due to clustering of AQP-5 at the microvilli (especially evident in the parotid gland) after 10 min of drug injection. No changes in the subcellular localization of AQP-5 were seen in response to epinephrine, atropine, or phentolamine treatment compared with control tissues. Thus AQP-5 is localized predominantly in the apical plasma membrane under control conditions, and neither the onset nor the cessation of secretion is associated in vivo with any significant short-term translocation of AQP-5 between intracellular structures and the apical plasma membrane.

show abstract

Section: Subcellular Localization Of Aqp-5 In Salivary Glands By Lighsupporting

confidence: 72%

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Gresz

Kwon

Gong

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…Preparation of rat parotid tissue Parotid glands were obtained from male Wistar rats (200-350 g) and small pieces of the tissue were prepared as described previously (Hata et al, 1983). Before experiments, Krebs-Ringer Tris (KRT) solution, consisting of (mM) NaCl 120, KCI 4.8, KH2PO4 1.2, MgSO4 1.2, CaCI2 3.0, Tris HC1 buffer (pH 7.4) 16 and glucose 5, was aerated with 02 and the pieces of parotid tissues were equilibrated with the solution for 20 min at 37°C with shaking.…”

Section: Methodsmentioning

confidence: 99%

Dopamine‐induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.

Hata

Ishida

Kondo

1986

British J Pharmacology

View full text Add to dashboard Cite

1 The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro.2 Dopamine induced marked amylase secretion from the tissue in a dose-dependent manner. Its EC50 value was about 4 gM and the maximal response was obtained at a concentration of 100 AM.3 The dopamine-induced secretion was inhibited by the dopamine-antagonists haloperidol, (+)-butaclamol and spiroperidol. 4 Atropine reduced the dopamine-induced secretion significantly, and physostigmine enhanced the secretion. 5 Parasympathectomy of the gland resulted in a significant decrease in the dopamine-induced secretion, but did not reduce the secretion induced by dopamine with atropine. 6 Dopamine-induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [3H]-choline. Dopamine elicited Ca2+-sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. 7 Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamineinduced secretion, but increase in noradrenaline (NA)-or isoprenaline-induced secretion. 8 Dopamine-induced NA release was studied by preloading the parotid tissue with [3H]-NA. Dopamine induced Ca2"-sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. 9 Several lines of circumstantial evidence strongly suggested that dopamine has a specific site for action in the parotid tissue that is independent of NA receptors. 10 In sympathectomized or reserpine-treated glands, atropine completely inhibited the dopamineinduced amylase secretion, suggesting that dopamine did not have a direct effect on postsynapses. 11 These findings indicate that dopamine induces amylase secretion in two indirect ways mediated through ACh and NA released from parasympathetic and sympathetic nerve terminals, respectively.

show abstract

“…Other methods and procedures were as described previously (1 ). Procaterol hydrochloride was a gift from Otsuka Pharmaceutical Co. (Tokushima, Japan), terbutaline sulfate was from Fujisawa Pharmaceutical Co. (Osaka, Japan), and prenalterol hydrochloride was from Hassle AB (Molndal, Sweden).…”

mentioning

confidence: 99%

“…The tissue was then washed well with KRT solution, transferred to fresh KRT solution for 10 min at 37'C (resting period), and then challenged by re incubation with the same agonist for 10 min (second incubation). (1). Cyclic AMP in tissues was measured by radioimmunoassay (2) with a Yamasa cyclic AMP assay kit (Yamasa Shoyu, Co., Chiba, Japan).…”

mentioning

confidence: 99%

“…and small pieces of the tissue were prepared as described previously (1). Before experiments, Krebs Ringer Tris (KRT) solution, consisting of 1 20 mM NaCI, 4.8 mM KCI, 1.2 mM KH2PO4, 1.2 mM MgSO4, 3.0 mM CaCI2, 16 mM Tris HCI buffer (pH 7.4) and 10 mM glucose, was aerated with 02 gas; and the pieces of parotid tissues were equilibrated with the solution for 20 min at 37'C with shaking.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Supersensitivity of Amylase Secretion from Rat Parotid Tissue—Its Selective Nature for the β2-Adrenergic Response

Hata

Noguchi

Ishikawa

et al. 1985

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

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

Cited by 38 publications

References 31 publications

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Immunolocalization of AQP-5 in rat parotid and submandibular salivary glands after stimulation or inhibition of secretion in vivo

Dopamine‐induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.

Supersensitivity of Amylase Secretion from Rat Parotid Tissue—Its Selective Nature for the β2-Adrenergic Response

Contact Info

Product

Resources

About