Substance P-induced diacylglycerol formation in rat parotid acinar cells

Komabayashi, Takao; Yakata, Atsushi; Izawa, Tetsuya; Suda, Kazuhiro; Noguchi, Masamichi; Tsuboi, Masahiro

doi:10.1016/0922-4106(91)90007-5

Cited by 6 publications

(5 citation statements)

References 28 publications

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“…Moreover, we obtained similar results after stimulation with sub stance P or carbachol (12,35). Perhaps, phosphatidyl ethanolamine hydrolysis may not be associated directly with DAG generation in the parotid gland.…”

Section: Discussionsupporting

confidence: 73%

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Sustained Changes in Acetylcholine and Amino Acid Contents of Brain Regions Following Microsphere Embolism in Rats

Taguchi

Miyake

Tanonaka

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-The kinetics and mechanism of sn-1,2-diacylglycerol (DAG) formation induced by isoprenaline were studied in rat parotid acinar cells. DAG accumulation induced by 100 pM isoprenaline reached its maximum at 1 min, rapidly decreased (about 50%) at 5 min and then remained constant for 30 min. DAG accumulation 1 min after isoprenaline treatment was dose-dependent. Either propranolol or phentolamine inhibited isoprenaline-stimulated DAG accumulation in a dose-dependent manner. Addition of a vasoactive intestinal polypeptide, forskolin, or dibutyryl cyclic AMP had no effect on DAG accumula tion. Isoprenaline did not cause the release of [3H]choline or [3H]ethanolamine metabolites into the medium. Based on the kinetics of DAG formation and [32P]phosphoinositide breakdown, we conclude that isoprenaline-induced DAG formation was mainly related to the hydrolysis of [32P]phosphatidylinositol 4,5 bisphosphate ([32P]PIP2). These results suggest that the effect of isoprenaline on DAG formation is mediated by a,-adrenoceptor activation, that it is not related to the increase in cyclic AMP, and that it is closely related to PIP2 hydrolysis.

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Section: Discussionsupporting

confidence: 73%

“…In the parotid gland, both PIP and PIP2, but not PI, are mainly hydrolyzed by phos pholipase C through receptor activation (12,28,29). In this study, the kinetics of DAG formation induced by 100 pM isoprenaline was very similar to that of [32p]PIP2 breakdown, but was not similar to those of [32P]PI and [32P]PIP breakdown (Fig.…”

Section: Discussionmentioning

confidence: 53%

Sustained Changes in Acetylcholine and Amino Acid Contents of Brain Regions Following Microsphere Embolism in Rats

Taguchi

Miyake

Tanonaka

et al. 1993

Japanese Journal of Pharmacology

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“…In parotid acini, substance P increases the intracellular concentration of diglycerides and amylase secretion at concentrations much higher than the concentrations required to increase the release of IPS and the [Ca2'li (Arkle et al, 1989). The effector coupled to these low affinity receptors remains unknown, but the fact that their occupancy increases the intracellular concentration of diglycerides (Komabayashi et al, 1991) suggests that they are coupled to the metabolism of phospholipids and triglycerides. It has been shown that high concentrations of substance P did not increase the release of choline or ethanolamine excluding a role for phospholipase D (Komabayashi et al, 1991).…”

Section: Frtl-5 Thyroid Cells Reported That Adenosine Agonistsmentioning

confidence: 99%

“…The effector coupled to these low affinity receptors remains unknown, but the fact that their occupancy increases the intracellular concentration of diglycerides (Komabayashi et al, 1991) suggests that they are coupled to the metabolism of phospholipids and triglycerides. It has been shown that high concentrations of substance P did not increase the release of choline or ethanolamine excluding a role for phospholipase D (Komabayashi et al, 1991). Rollandy et al (1991) reported that the doseresponse curve of substance P for amylase release from parotid acini was biphasic.…”

Section: Frtl-5 Thyroid Cells Reported That Adenosine Agonistsmentioning

confidence: 99%

Low affinity purinergic receptor modulates the response of rat submandibular glands to carbachol and substance P

et al. 1996

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The effect of extracellular ATP on the intracellular calcium concentration ([Ca2+]i) in rat submandibular glands was tested. The dose-response curve for ATP was biphasic with a first increase in the 1-30 microM concentration range and a further increase at concentrations higher than 100 microM. Among ATP analogs, only benzoyl-ATP stimulated the low affinity component. ATP tau S blocked this response. All the other analogs tested reproduced the high-affinity low capacity response. Magnesium and Coomassie blue selectively blocked the low affinity component. High concentrations of ATP blocked the increase of the intracellular calcium concentration [Ca2+]i in response to 100 microM carbachol. By itself, substance P (100 pM-1 microM) increased the [Ca2+]i. One mM ATP potentiated the response to concentrations of substance P higher than 10 nM. This potentiation was reversed by extracellular magnesium. Carbachol 100 microM and substance P (100 pM-1 microM) increased the release of inositol trisphosphate (IP3) from polyphosphoinositides (polyPI). Activation of the low affinity ATP receptors did not activate the polyPI-specific phospholipase C but inhibited its activation by 100 microM carbachol (-50%) and by 100 nM substance P (-60% at 1 nM substance P and -40% at 100 nM substance P). Substance P induced a strong homologous desensitization: a preincubation with 1 nM substance P nearly completely abolished the response to 1 microM substance P. When the cells were exposed to ATP before the second addition of substance P, the purinergic agonist partially restored the response to the tachykinin without totally reversing the desensitization. It is concluded that two types of purinergic receptors coexist in rat submandibular glands; a high-affinity, low capacity receptor which remains pharmacologically and functionally undefined and a low affinity site, high capacity receptor of the P2z type coupled to a non-selective cation channel. The occupancy of these low affinity sites blocks the increase of the [Ca2+]i in response to a muscarinic agonist and the activation of polyPI-specific phospholipase C by carbachol and substance P. It potentiates the effect of high concentrations of substance P on the [Ca2+]i.

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“… G s and G q [ 241 - 243 ]. ↑ intracellular Ca 2+ , DAG, cAMP, IP3 [ 79 , 239 , 244 - 246 ]. CFTR has been implicated [ 100 ].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptides in asthma, chronic obstructive pulmonary disease and cystic fibrosis

Atanasova

Reznikov

2018

Respir Res

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The nervous system mediates key airway protective behaviors, including cough, mucus secretion, and airway smooth muscle contraction. Thus, its involvement and potential involvement in several airway diseases has become increasingly recognized. In the current review, we focus on the contribution of select neuropeptides in three distinct airway diseases: asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. We present data on some well-studied neuropeptides, as well as call attention to a few that have not received much consideration. Because mucus hypersecretion and mucus obstruction are common features of many airway diseases, we place special emphasis on the contribution of neuropeptides to mucus secretion. Finally, we highlight evidence implicating involvement of neuropeptides in mucus phenotypes in asthma, COPD and cystic fibrosis, as well as bring to light knowledge that is still lacking in the field.

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Substance P-induced diacylglycerol formation in rat parotid acinar cells

Cited by 6 publications

References 28 publications

Sustained Changes in Acetylcholine and Amino Acid Contents of Brain Regions Following Microsphere Embolism in Rats

Sustained Changes in Acetylcholine and Amino Acid Contents of Brain Regions Following Microsphere Embolism in Rats

Low affinity purinergic receptor modulates the response of rat submandibular glands to carbachol and substance P

Neuropeptides in asthma, chronic obstructive pulmonary disease and cystic fibrosis

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