Effects of bradykinin, GTPγS, R59022 and N-ethylmaleimide on inositol phosphate production in NG108-15 cells

Chiang, Chaung-Fu; Hauser, George

doi:10.1016/0006-291x(89)91051-6

Cited by 9 publications

(2 citation statements)

References 37 publications

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“…R 59 022 has been shown to enter cells and inhibit diacylglycerol kinase (de Chaffoy de Courcelles et al, 1985) and we have shown that under the conditions used here the inhibitor does elevate the levels of diacylglycerol in chromaffin cells (Owen and Boarder,199 1). In NG 108-1 5 cells and neutrophils, R 59 022 can stimulate inositol phosphate metabolism thereby increasing diacylglycerol production (Mahadevappa, 1988;Chiang and Hauser, 1989). Also, the observation that nicotine-and high potassium-stimulated noradrenaline release was inhibited by R 59 022 whereas bradykinin-stimulated noradrenaline release was not (Owen and Boarder,199 1 ), seemed to suggest a role for phosphatidic acid in stimulus-secretion coupling.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, doubt has been cast on the specificity of this inhibitor. In NG 108-1 5 cells and neutrophils, R 59 022 can stimulate inositol phosphate metabolism thereby increasing diacylglycerol production (Mahadevappa, 1988;Chiang and Hauser, 1989). However, others have failed to observe effects on either inositol phospholipid breakdown or Ca2+ entry (Nunn and Watson, 1987), although Mege et al (1988) reported a small but significant increase in intracellular calcium with R 59 022 alone.…”

Section: Discussionmentioning

confidence: 99%

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Phosphatidic Acid Accumulation and Catecholamine Release in Adrenal Chromaffin Cells: Stimulation by High Potassium and by Nicotine, and Effect of a Diacylglycerol Kinase Inhibitor R 59 022

Owen

Jones

Boarder

1991

Journal of Neurochemistry

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Using primary cultures of bovine adrenal chromaffin cells labelled with 32Pi, we show that stimulation with bradykinin, nicotine, or a depolarising concentration of potassium stimulates the accumulation of [32P]phosphatidic acid. The effects of nicotine and potassium are smaller than the effect of bradykinin, and are dependent entirely on extracellular calcium. The diacylglycerol kinase inhibitor R 59 022 attenuates the formation of phosphatidic acid by nicotine and depolarising concentrations of potassium. This inhibitor also blocks the nicotine and potassium stimulation of noradrenaline release from chromaffin cells. Using 45Ca2+ influx studies, we show that the nicotine-evoked calcium influx is also attenuated by R 59 022. These observations contrast with those in another report in which we showed that bradykinin stimulation of either [32P]phosphatidic acid accumulation or noradrenaline release is not affected by R 59 022. It is likely that the calcium influx produced by nicotine and depolarising potassium is blocked by R 59 022 by a mechanism that is independent of its ability to block diacylglycerol kinase. The nicotine- and potassium-stimulated [32P]phosphatidic acid accumulation is a consequence of this calcium influx and presumably reflects calcium activation of either phospholipase C or phospholipase D.

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Section: Discussionmentioning

confidence: 99%