Adenine-Derived Purines Increase Adenosine Triphosphate (ATP) Levels in the Luteal Cell: Evidence that Cell Levels of ATP May Limit the Stimulation of Adenosine 3′5′-Monophosphate Accumulation by Luteinizing Hormone*

Brennan, Thomas J.; Ohkawa, Reiko; Gore, Steven D.; Behrman, Harold R.

doi:10.1210/endo-112-2-499

Cited by 35 publications

(13 citation statements)

References 12 publications

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“…The time course and extent of the adenosine-induced increase in the concentration .of ATP in the ovaries were similar to those obtained in isolated luteal cells (7). This suggests that in isolated luteal cells a loss of ATP may have occurred during the multistep isolation procedure, which was reversed by adenosine.…”

Section: Discussionsupporting

confidence: 75%

³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

Haseltine

Arias‐Mendoza

Kaye

et al. 1986

Magnetic Resonance in Med

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Section: Discussionsupporting

confidence: 75%

³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

Haseltine

Arias‐Mendoza

Kaye

et al. 1986

Magnetic Resonance in Med

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“…Adenosine produces a large increase in luteal cell ATP content (11,19). Also, mitochondrial oxidative phosphorylation and ATP production are necessary for amplification by adenosine of LH-stimulated cAMP accumulation (3).…”

Section: Discussionmentioning

confidence: 99%

“…The decrease in cellular ATP levels was not unexpected, because it is well known that increasing cellular calcium levels cause increased ATP utilization and decreased ATP production (23,24). Since luteal cell ATP content is an important factor in the regulation of LH-stimulated cAMP production (3,11), it was important to determine whether the effect of ionomycin on luteal cell cAMP accumulation was due to increased cellular calcium levels or to decreased cellular ATP levels. Cholera toxin-stimulated cAMP and ATP levels were both decreased by ionomycin.…”

Section: Discussionmentioning

confidence: 99%

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Selective Amplification of Luteinizing Hormone by Adenosine in Rat Luteal Cells*

1988

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Adenosine amplification of LH-stimulated cAMP accumulation in rat luteal cells is rapid and dependent on mitochondrial ATP production. The objective of the present studies was to determine if this effect of adenosine is specific for LH and to gain information on the mechanism of the ATP-dependent amplification of LH action in rat luteal cells. Adenosine significantly amplified maximum cAMP accumulation in response to LH, isoproterenol, forskolin, and cholera toxin. However, amplification of this response by adenosine was significantly greater for LH than for the other agonists. The relative order of amplification by adenosine was LH greater than isoproterenol greater than forskolin greater than cholera toxin; the relative magnitudes of amplification by adenosine were 1, 0.6, 0.2, and 0.2, respectively. Neither LH, isoproterenol, forskolin, nor cholera toxin had any effect on cellular levels of ATP, and adenosine produced a similar rate of increase and maximal levels of ATP in the presence of all agonists. Ionomycin, a calcium ionophore, inhibited LH- and cholera toxin-stimulated cAMP accumulation and produced a dose-dependent depletion of ATP. Adenosine reversed the inhibitory effect of ionomycin on LH-stimulated cAMP accumulation and cellular levels of ATP. However, adenosine did not reverse the inhibitory effect of ionomycin on cholera toxin-stimulated cAMP accumulation, although its effects on cellular ATP levels were identical to those on LH. Thus, the selective amplification of LH by adenosine is not merely a substrate effect on adenylate cyclase activity. The nature of adenylate cyclase activation by cholera toxin and forskolin and the weak amplification by adenosine of these agonists compared to that of LH indicate that the site of the ATP-dependent action of adenosine appears to be before or on the G-protein of adenylate cyclase. We suggest that adenosine, by an ATP-dependent process, either increases the availability of functional LH receptors or increases coupling between the LH receptor and adenylate cyclase.

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“…1 and 2 were performed after 60 min of preincubation at 0.78 mM phosphate without metabolic substrates, the ATP content in the Hyp mice was significantly lower than that in the normal mice, resulting in the lower cAMP generation. By raising the ATP content with the phosphate or substrate supplementation, the cAMP generation was greatly enhanced in Hyp mice compared with the normal controls, 26 suggesting that the utilization efficiency of ATP for adenylate cyclase is enhanced in Hyp mice. Thus, Fig.7 is not contradictory to Figs.…”

Section: Ionized Calcium Levelsmentioning

confidence: 99%

Blunted effect of parathyroid hormone on adenosine 3′,5′-cyclic monophosphate production is derived from ATP depletion in proximal convoluted tubules of hypophosphatemic mice

Shima

Yamaoka

Nakamura

et al. 2000

Clinical and Experimental Nephrology

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Background.To clarify the pathophysiological features associated with phosphate depletion in hypophosphatemic (Hyp) mice, we examined the effect of extracellular phosphate on parathyroid hormone (PTH)-stimulated adenosine 3Ј,5Ј-cyclic monophosphate (cAMP) production in the proximal convoluted tubules (PCT). Methods. PTH-Stimulated cAMP production and ATP content were determined by radioimmunoassay and luciferinluciferase chemiluminescence methods, respectively. Results. The level of cAMP stimulated by PTH at an extracellular phosphate concentration of 0.78 mM was lower in the Hyp mice than in normal mice. The PTH-stimulated cAMP production in the Hyp mice was increased when the extracellular phosphate concentration was raised. In contrast, an increase in extracellular phosphate did not affect the PTH-stimulated cAMP production in the normal mice. Although the ATP content of the PCT was not different between the normal and Hyp mice immediately after microdissection, after 60 min of incubation, it had decreased to a greater extent in Hyp mice than in the normal animals. Raising the extracellular phosphate concentration from 0.78 to 2.3 mM prevented the decrease in ATP content in Hyp mice, and the intracellular ATP content then became comparable to that in the normal control. Conclusions. These results suggest that ATP content in the PCT tended to be decreased in Hyp mice by a decreased phosphate supply and that the blunted effect of PTH on cAMP production in these mice is due to ATP depletion.

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Adenine-Derived Purines Increase Adenosine Triphosphate (ATP) Levels in the Luteal Cell: Evidence that Cell Levels of ATP May Limit the Stimulation of Adenosine 3′5′-Monophosphate Accumulation by Luteinizing Hormone*

Cited by 35 publications

References 12 publications

³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

Selective Amplification of Luteinizing Hormone by Adenosine in Rat Luteal Cells*

Blunted effect of parathyroid hormone on adenosine 3′,5′-cyclic monophosphate production is derived from ATP depletion in proximal convoluted tubules of hypophosphatemic mice

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Adenine-Derived Purines Increase Adenosine Triphosphate (ATP) Levels in the Luteal Cell: Evidence that Cell Levels of ATP May Limit the Stimulation of Adenosine 3′5′-Monophosphate Accumulation by Luteinizing Hormone*

Cited by 35 publications

References 12 publications

31P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

31P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

Selective Amplification of Luteinizing Hormone by Adenosine in Rat Luteal Cells*

Blunted effect of parathyroid hormone on adenosine 3′,5′-cyclic monophosphate production is derived from ATP depletion in proximal convoluted tubules of hypophosphatemic mice

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³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries

³¹P NMR studies of adenosine‐stimulated ATP synthesis in perfused luteinized ovaries