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SUMMARY
The role of cyclic AMP in the mediation of hormone action is reviewed, including information available from 1958–1971. Evidence for its involvement in each hormone action is considered separately. The known mechanisms by which cyclic AMP stimulates specific metabolic processes are also described. Other speculations on the role of cyclic AMP in the mediation of hormone action are discussed.
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Adrenocortical cyclic AMP (both total and protein-bound), and adrenal and plasma concentrations of corticosterone were measured in male rats killed at selected intervals throughout the day. The animals had previously been synchronized for 3 weeks in natural lighting. Adrenal and plasma levels of corticosterone showed similar circadian fluctuations and the onset of their ascending phases started at 13.00 h, maximum concentrations being reached at 21.00 h. On the other hand, a time-lag between the circadian variations of total cyclic AMP and protein-bound cyclic AMP could be seen in adrenocortical tissue. The onset of an increase in adrenocortical protein-bound cyclic AMP was apparent at 15.00 h and the peak occurred at 21.00 h, while total adrenocortical cyclic AMP did not begin to rise before 19.00 h and was maximal at 04.00 h. No direct link between total cyclic AMP and protein-bound cyclic AMP could be seen during the dark phase, suggesting a functional compartmentalization of cyclic AMP in the adrenal gland of the rat. While the ascending phase of the rhythm in steroidogenesis preceded the rise in total adrenocortical cyclic AMP by about 4 h an excellent synchrony between the respective patterns of corticosterone concentration and protein-bound cyclic AMP was noticed.
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SUMMARY
The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex.
Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.
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ABSTRACT
We have studied the effects of cyclic AMP (cAMP) on TSH secretion by cultured rat pituitary cells, using forskolin and dibutyryl cAMP (dbcAMP) to raise the cellular cAMP content by different mechanisms. Forskolin (10 μmol/l), a stimulator of adenylate cyclase, raised the cAMP content within 10 min, but had a more delayed effect on TSH release, with no significant stimulation for at least 6 h, but a clear dose-dependent effect at 24 h. Incubation with dbcAMP likewise increased TSH release after 6–24 h. By contrast, high cellular cAMP levels induced by either forskolin or dbcAMP augmented the TSH response to TRH at an early stage, before any detectable change in unstimulated TSH release. Pretreatment of cells with forskolin led to a parallel upward shift in the subsequent TRH dose-response curve, without a significant change in median effective dose or any change in cellular TSH content.
These findings suggest that cAMP acts to increase the availability of TSH for acute release by TRH by modulation of an intracellular releasable hormone pool, and indicate synergistic interactions between the adenylate cyclase system and the phospholipid-calcium stimulus-release coupling mechanism of TRH.
J. Endocr. (1986) 109, 365–369
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ABSTRACT
The effect of dibutyryl cyclic AMP and FSH on oestrogen biosynthesis was investigated in testes from 18- to 21-day-old fetal rats cultured in vitro in the presence of tritiated testosterone. Oestrone and oestradiol concentrations were measured by determination of constant specific activity after isotopic dilution.
Dibutyryl cyclic AMP and FSH markedly stimulated the conversion of testosterone into both oestrone and oestradiol at all stages studied. Oestradiol synthesis was stimulated by two- to sevenfold, while stimulation of oestrone synthesis was even greater. The results demonstrate that the aromatase enzyme system of the fetal rat testis responds to cyclic AMP and FSH.
J. Endocr. (1988) 118, 485–489
Search for other papers by D. B. COOK in
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Search for other papers by G. A. SMART in
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SUMMARY
The effect of intravenous infusions of ATP and dibutyryl cyclic AMP (DB cyclic AMP) on adrenocorticotrophin (ACTH) and corticosteroid release was investigated in piglets.
A consistent increase of both plasma ACTH and plasma cortisol was observed in response to infusions of 600 mg ATP/h. These responses were abolished by pretreating the animals with dexamethasone. A similar pattern of response was observed with DB cyclic AMP infused intravenously. No response occurred when 100 mg DB cyclic AMP were infused in 1 h, but there was a marked plasma corticosteroid response to an infusion of 600 mg DB cyclic AMP in 1 h. Surprisingly, this response was also abolished by pretreatment with dexamethasone.
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Cátedra de Fisiología con Biofísica, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60y 120, 1900 La Plata, Argentina
(Received 23 July 1976)
There is general agreement that glucose-induced insulin release is mediated by a complex mechanism (Randle & Hales, 1972). It has also been postulated that cyclic AMP might play an important role in this process. However, conflicting results have been reported about the effect of glucose on cyclic AMP levels in the islets of Langerhans (Charles, Fanska, Schmid, Forsham & Grodsky, 1973; Cooper, Ashcroft & Randle, 1973). Since it has been shown that cyclic AMP release from the liver rather than its intracellular concentration is better related to some metabolic effects (Exton & Park, 1972), we felt that a similar correlation might exist in the β cell. The release of both insulin and cyclic AMP by isolated islets was measured in the presence of various glucose concentrations.
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Porcine relaxin produced a rapid, dose-related rise of cyclic AMP values in rat uterine tissue incubated in vitro. In time-course experiments, peak cyclic AMP concentrations were observed in the uterine slices at 5 min; subsequently the values fell, at first rapidly and then more slowly with the tissue concentration remaining significantly raised at 15 min. Levels of cyclic GMP in the same tissue slices were not significantly altered by relaxin. Furthermore, no increase in basal cyclic AMP values was measured in control slices prepared from the rat heart or jejunum. An increase in cyclic AMP concentration comparable to that found in the rat uterus was observed in slices of porcine uterus and cervix but not of vagina when they were stimulated with porcine relaxin. Our results suggest that the hormonal action of relaxin on the uterus and cervix is mediated through receptors linked to the enzyme, adenylate cyclase.
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SUMMARY
Primary tissue cultures of adrenal cells were prepared from foetal rat adrenals. The effect of cyclic AMP (75 μmol/l) on the morphology and steroid synthetic activity of the cortical cells was examined in order to determine whether cyclic AMP mimics the effects induced by adrenocorticotrophin (ACTH); namely transformation to the differentiated cell type and increase in steroid synthetic activity. Cyclic AMP was found to induce some, but not all, of the changes normally induced by ACTH. In particular, the mitochondria in the cortical cells developed vesicular cristae and there was a proliferation of the smooth endoplasmic reticulum. These two organelles are the principle sites of enzymes involved in steroid synthesis and the ultrastructural transformation was accompanied by an increase in the steroidogenic activity of the cells. However, clear differences in the ultrastructure of the cyclic AMP- and ACTH-treated cells were noted. The effects of cyclic AMP on the ultrastructure of cortical and fibroblastic cells present in the adrenal cultures were found to be dependent upon the cell type.
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Department of Medicine and Biochemistry Research Group, University of Otago Medical School, Dunedin, New Zealand
(Received 7 October 1974)
High doses of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) inhibit bone mineralization, induce hypercalcaemia and diminish intestinal absorption of calcium in the rat (Gasser, Morgan, Fleisch & Richelle, 1973; Goulding & McChesney, 1974). This hypercalcaemia, either by a direct effect or by inhibiting secretion of parathyroid hormone (PTH), may suppress renal synthesis of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and hence explain the diminished intestinal absorption of calcium (Bonjour, DeLuca, Fleisch, Trechsel, Matejowee & Omdahl, 1973; Hill, Lumb, Mawer & Stanbury, 1973). Parathyroid hormone affects the renal production and excretion of cyclic AMP (Chase & Aurbach, 1967) and cyclic AMP enhances the synthesis of 1,25(OH)2D3 (Rasmussen, Wong, Bikle & Goodman, 1972; Larkins, MacAuley, Rapoport, Martin, Tullock, Byfield, Matthews & Maclntyre, 1974). Thus reduced production of cyclic AMP after administration of EHDP may be important in diminishing renal synthesis
