β1-Adrenergic Regulation of Cyclic Nucleotide Levels and Potassium Fluxes in Rat Parotid Gland

Miyamoto, Atsushi; Ohshika, Hideyo

doi:10.1254/jjp.36.100

Cited by 4 publications

(1 citation statement)

References 14 publications

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“…Our results suggest that some P2-receptors in the submandibular gland might not play a role in potentiating the substance P-mediated secretion of fluid. The potentiating effects of the three agonists tested were consistent with those reported by Miyamoto & Ohshika (1984) and Suzuki & Ohshika (1985), who found that the potency of /3-adrenergic agonists with regard to the production of CAMP in rat parotid tissue was isoprenaline >> dobutamine > procaterol. Larsson & Olgart (1989) reported that forskolin, which increases levels of CAMP via its action on adenylate cyclase, augments the carbachol-evoked secretion of fluid from the rat parotid gland.…”

Section: Discussionsupporting

confidence: 89%

Interaction Between Substance P and β-Adrenergic Agonists in the Modulation of the Secretion of Fluid and Protein by the Rat Submandibular Gland

Iwabuchi

Kimura

1998

Journal of Pharmacy and Pharmacology

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The interactions between substance P and beta-adrenergic agonists such as isoprenaline, dobutamine and terbutaline in the control of the secretion of fluid and protein from the rat submandibular gland have been examined. Substance P elicited large volumes of saliva whereas isoprenaline, dobutamine and terbutaline elicited small volumes only. The secretion of fluid in response to substance P was markedly enhanced when substance P was administered in combination with isoprenaline or dobutamine but not when it was administered in combination with terbutaline. Isoprenaline elicited large amounts of protein, whereas substance P elicited small amounts. The secretion of protein in response to isoprenaline did not change when isoprenaline was administered in combination with substance P. The secretion of fluid and protein induced by substance P in combination with isoprenaline was antagonized by metoprolol and by spantide, but it was unaffected by pretreatment with ICI118551. These results suggest that in the rat submandibular gland stimulation of beta1-adrenoceptors but not of beta2-adrenoceptors potentiates the secretion of fluid that is induced by stimulation of tachykinin receptors, whereas stimulation of tachykinin receptors does not enhance the secretion of protein that is induced by stimulation of beta1-adrenoceptors.

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Section: Discussionsupporting

confidence: 89%

Interaction Between Substance P and β-Adrenergic Agonists in the Modulation of the Secretion of Fluid and Protein by the Rat Submandibular Gland

Iwabuchi

Kimura

1998

Journal of Pharmacy and Pharmacology

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Enhancement of Stimulation‐Evoked Catecholamine Release from Cultured Bovine Adrenal Chromaffin Cells by Forskolin

Morita

Dohi

Kitayama

et al. 1987

Journal of Neurochemistry

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Acetylcholine (ACh) increased cyclic AMP levels in cultured bovine chromaffin cells with a peak effect at 1 min after the addition. Pretreatment with forskolin (0.3 microM) enhanced the ACh-evoked cyclic AMP increase. The catecholamine (CA) release induced by ACh was enhanced by forskolin, but forskolin alone did not enhance the CA release. The effect of forskolin increased dose-dependently up to 1 microM, but decreased at higher concentrations. Dibutyryl cyclic AMP (DBcAMP) also enhanced ACh-evoked CA release, but the effect was less potent than that of forskolin. Forskolin enhanced both [3H]norepinephrine ([3H]NE) and endogenous CA release evoked by 30 mM K+ from cells that were preloaded with [3H]NE. The effects of forskolin were substantial when CA release was evoked with low concentrations of ACh or excess K+, but decreased with higher concentrations of the stimulants. Forskolin also enhanced the CA release induced by ionomycin and veratrine, or by caffeine in Ca2+-free medium. The potentiation by forskolin of the ACh-evoked CA release was manifest in low Ca2+ concentrations in the medium, but decreased when Ca2+ concentration was increased. These results suggest that cyclic AMP may play a role in the modulation of CA release from chromaffin cells.

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Isoproterenol Inhibition of Potassium Release from Rat Parotid Gland

Miyamoto

Ohshika

1985

Japanese Journal of Pharmacology

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Abstract-The mechanism of isoproterenol-induced inhibition of potassium release from rat parotid slices has been determined. Spontaneous potassium release from the slices was significantly inhibited by isoproterenol at concentrations above 10-6 M. This isoproterenol effect was completely abolished in the presence of propranolol (10-5M) and ouabain (10-3 M) and was abolished during Na+-exclusion from the incubation medium.Isoproterenol caused an enhancement of the micro somal Na+, K+-ATPase activity at concentrations above 10-5 M, and this activity was inhibited by propranolol (10-5 M). The stimulatory effect of isoproterenol on the Na+, K+-ATPase exhibited a strong correlation with the inhibition of potassium release on each dose of isoproterenol.Moreover, dibutyryl cyclic AMP at concen trations above 10-4 M inhibited potassium release in a dose-dependent manner and cyclic AMP caused an enhancement of the microsomal Na+, K+-ATPase activity. These results suggest that the inhibitory effect of isoproterenol on potassium release is clearly derived from the elevated Na+, K+-ATPase activity and that it may in part be mediated by cyclic AMP.

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β1-Adrenergic Regulation of Cyclic Nucleotide Levels and Potassium Fluxes in Rat Parotid Gland

Cited by 4 publications

References 14 publications

Interaction Between Substance P and β-Adrenergic Agonists in the Modulation of the Secretion of Fluid and Protein by the Rat Submandibular Gland

Interaction Between Substance P and β-Adrenergic Agonists in the Modulation of the Secretion of Fluid and Protein by the Rat Submandibular Gland

Enhancement of Stimulation‐Evoked Catecholamine Release from Cultured Bovine Adrenal Chromaffin Cells by Forskolin

Isoproterenol Inhibition of Potassium Release from Rat Parotid Gland

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