Factors affecting the saturation assay of cyclic AMP in biological systems

Albano, J. D. M.; Barnes, Godfrey; Maudsley, David V.; Brown, Barry L.; Etkins, Roger P.

doi:10.1016/0003-2697(74)90137-7

Cited by 72 publications

(7 citation statements)

References 9 publications

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“…(2) A similar comparison with the ethanol extraction method proposed by others (Albano, Barnes, Maudsley et al 1974) gave a ratio of 1-126 ±0-060 (n = 9), also very close to 1, between 0 and 10 pmol cAMP in the samples.…”

Section: Preparation Of Hepatocytessupporting

confidence: 66%

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

Lahlou¹,

Fossat²,

Porthé-Nibelle³

et al. 1988

Journal of Endocrinology

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Cyclic AMP levels were measured in freshly isolated hepatocytes of the rainbow trout. Compared with basal values, the average levels were increased up to 60 times in a dose-dependent manner either by mammalian glucagon (concentration range 1 nmol-1 mumol/l; dose giving half maximum response (EC50) 0.18 mumol/l) or by forskolin (concentration range 0.1-100 mumol/l; EC50 about 10 mumol/l). These stimulatory effects were partially inhibited by fish or mammalian neurohypophysial hormones used at relatively high concentrations (1-5 mumol/l). It is suggested that these results are evidence for the presence of V1-type receptors in fish hepatocytes. Together with previous results obtained with gills on the hormonal inhibition of adenylate cyclase activity, they suggest that teleost fish may possess only V1-type receptors (or two V1-related types), while the V2 receptors have evolved (or have become functional) in higher vertebrates.

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Section: Preparation Of Hepatocytessupporting

confidence: 66%

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

Lahlou¹,

Fossat²,

Porthé-Nibelle³

et al. 1988

Journal of Endocrinology

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“…The dried sample was reconstituted with assay buflFer (50 mM Tris-HCl, pH 7-4, 8 niM theophylline, 6 niM 2-mercaptoethanol) (i ml). Aliquots (50 /d) of this solution were assayed for cyclic AMP using the saturation assay method of Brown et al (1971) and Albano et al (1974). The specificity ofthe assay was determined by the removal of cyclic AMP using cyclic nucleotide phosphodiesterase (Voorhees ei aL, 1972).…”

Section: Estimation Of Cyclic Amp (Adenosine-^\ $'-Cyclic Monophosphate)mentioning

confidence: 99%

The relationship between cyclic adenosine 3',5'-monophosphate and biochemical events in rat skin after the induction of epidermal hyperplasia using hexadecane

Peters¹,

White²

1978

Br J Dermatol

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Sequential changes in skin metabolism have been studied in a model system of epidermal hyperplasia and hyperkeratinization induced by the application of n-hexadecane to shaved rat skin. The epidermal accumulation of glycogen typical of the hyperplastic response has been correlated with an increase in glycogenesis and a decrease in glycogenolysis. DNA synthesis was increased by 6 h after the start of hexadecane treatment and reached a maximum after one day. The concentration of skin cyclic AMP fell immediately after hexadecane application and subsequently rose to give a prolonged increase. Use of the combined topical application of hexadecane and the anti-inflammatory drugs triamcinolone acetonide, hydrocortisone and indomethacin showed that the hexadecane-induced changes in DNA synthesis and glycogen metabolism were linked to the initial fall in cyclic AMP concentration. The significance of the biphasic change in cyclic AMP levels is discussed as a possible system of control for the development and maintenance of hyperplasia.

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“…They yielded very crude homogenates of the skin and resulted in a high coefficient of variation for replicates in individual cyclic AMP determinations. This variation can be partly attributed to interference by perchloric acid and trichloroacetic acid in the assay (Cooper, McPherson & Schofield, 1972;Albano, Barnes, Maudsley, Brown & Ekins, 1974). However, after boiling it was easy to homogenize the tissue and there was no variation in replicate cyclic AMP determinations.…”

mentioning

confidence: 99%

Endogenous prostaglandins, adenosine 3':5'‐monophosphate and sodium transport across isolated frog skin.

Hall¹,

O'Donoghue²,

O'Regan³

et al. 1976

The Journal of Physiology

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1. Sodium transport across isolated frog skin, as measured by the short-circuit current, was decreased by acetylsalicylic acid, mefenamic acid, paracetamol and phenylbutazone. Indomethacin (6 x 106 M) had a biphasic effect on the short-circuit current: a transient increase followed by a sustained decrease. 2. The release of prostaglandin-like material from the skin was reduced by acetylsalicylic acid and indomethacin. Paracetamol caused a significant reduction in the short-circuit current response of the skin to low doses of arachidonic acid, but the response to the highest dose tested was not significantly altered. 3. Indomethacin (6 x 106 M) increased the sensitivity of the skin to applied prostaglandin E1. The other prostaglandin synthetase inhibitors did not have this effect. Indomethacin (6 x 106 M) also enhanced the effect of antidiuretic hormone on the short-circuit current. 4. Indomethacin (30 x 106 M) increased the short-circuit current and diminished the response to applied prostaglandin E1. 5. In sulphate Ringer, theophylline increased the short-circuit current and diminished the response to prostaglandin E1. 6. Prostaglandin E1 increased the levels of cyclic AMP in frog skin and these increases preceded the increases in short-circuit current. There was a seasonal variation in the level of cyclic AMP in the skin: the levels in winter exceeded those in summer. There was also a seasonal variation in the cyclic AMP response to prostaglandin E1: the winter response was greater than that in summer. 7. Indomethacin (6 x 106 M) had a biphasic effect on cyclic AMP levels in the skin, an initial increase followed by a decrease. Indomethacin also potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 8. Theophylline increased cyclic AMP levels in the skin and potentiated prostaglandin E1 stimulated cyclic AMP accumulation. W. J. HALL AND OTHERS 9. Pre-treatment of the skin with theophylline reversed the effects of cyclic AMP on the short-circuit current and open-circuit potential. 10. It is concluded that endogenous prostaglandins help to maintain sodium transport across isolated frog skin and that the effects of E-type prostaglandins on the short-circuit current are mediated by increased cyclic AMP levels. The transient increase in short-circuit current and the increased skin sensitivity caused by indomethacin (6 x 10-6 mI) are attributed to inhibition of phosphodiesterase activity. The failure of theo-phylline to potentiate the short-circuit current response of the skin to prostaglandin E1 is attributed to alteration of cyclic AMP action on the skin by theophylline.

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Factors affecting the saturation assay of cyclic AMP in biological systems

Cited by 72 publications

References 9 publications

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

The relationship between cyclic adenosine 3',5'-monophosphate and biochemical events in rat skin after the induction of epidermal hyperplasia using hexadecane

Endogenous prostaglandins, adenosine 3':5'‐monophosphate and sodium transport across isolated frog skin.

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