Evidence for a Role of Adenosine 3′, 5′–Monophosphate in Parathyroid Hormone Release

Williams, George C.; Hargis, G. K.; Bowser, E. N.; Henderson, W. J.; Martinez, Norberto J.

doi:10.1210/endo-92-3-687

Cited by 98 publications

(41 citation statements)

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“…Because the technique used to measure the rate of bovine PTH secretion in vitro and the application of this technique to study PTH secretion have been described previously (18)(19)(20) 1-34 was significantly greater than zero, and the slope of % B/F as a function of molar concentration of bovine PTH 1-84 was significantly greater than the slope with bovine PTH 1-34. Therefore, because both standards exhibited competition with tracer and because bovine PTH 1-84 exhibited greater competition than bovine PTH 1-34, this antiserum detects both amino and carboxyl terminals of bovine PTH.…”

Section: Introductionmentioning

confidence: 99%

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Chertow¹,

Baylink²,

Wergedal³

et al. 1975

J. Clin. Invest.

213

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A B S T R A C T The present study determined the effects of 1,25-dihydroxycholecalciferol on serum immunoreactive parathyroid hormone and on parathyroid hormone secretion in vitro. Rats injected i.p. with 1,25-dihydroxycholecalciferol, 130 pmol (2 U)/140 g body wt, which is probably a physiologic dose, had a significant 43% decrease in serum immunoreactive parathyroid hormone at 4 h. In addition, this dose of 1,25-dihydroxycholecalciferol inhibited the serum immunoreactive parathyroid hormone response to hypocalcemia induced by phosphate injection. Because the increment in serum immunoreactive parathyroid hormone was less but the decrement in serum calcium more in phosphate plus 1,25-dihydroxycholecalciferol-treated than in phosphate plus vehicle-treated rats, the impaired serum immunoreactive parathyroid hormone response to 1,25-dihydroxycholecalciferol could not be attributed to the change in serum calcium. In studies of parathyroid hormone secretion from bovine parathyroid tissue in vitro, the concentration of 1,25-dihydroxycholecalciferol used for most experiments was 1 nM, which is in the range found in rat serum. 1,25-Dihydroxycholecalciferol at 1 or 100 nM significantly inhibited parathyroid hormone secretion when medium calcium concentration was normal (1.5 mM), high (3.0 mM), and low (1.0 mM).

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Section: Introductionmentioning

confidence: 99%

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Chertow¹,

Baylink²,

Wergedal³

et al. 1975

J. Clin. Invest.

213

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“…There is evidence from the study of parathyroid explants in vitro that the addition of catecholamines, dibutyryl cyclic adenosine 3',5'-monophosphate (cyclic AMP), and thyrocalcitonin to the incubation medium stimulates PTH secretion (6)(7)(8)(9) 16 min after the start of the infusions. When the effects of epinephrine were compared with epinephrine-plus-calcium and epinephrine-plus-propranolol, epinephrine was infused from time "0" to 7.0 min and from 60.0 to 67.0 min.…”

Section: Introductionmentioning

confidence: 99%

Acute Parathyroid Hormone Response to Epinephrine In Vivo

Fischer¹,

Blum²,

Binswanger³

1973

J. Clin. Invest.

153

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A B S T R A C T The acute effects of epinephrine, norepinephrine, and isoproterenol on the plasma immunoreactive parathyroid hormone (iPTH) response were studied in 13 550-600 kg cows. Catecholamines were infused for 7.0 min. During epinephrine infusions at 0.08 Amol/min iPTH increased from 0.48±0.12 (mean+SE, ng/ml) to 1.09±0.18 ng/ml (P < 0.02). Small increases in plasma free fatty acids and glucose could be detected with 0.08 Amol/min epinephrine; the iPTH response to epinephrine was as sensitive as the free fatty acid and glucose responses and possibly of physiological importance. Plasma calcium (total and ionized) and magnesium did not change.The responses were more pronounced at 0.8 /mol/min epinephrine with a mean iPTH increase from 0.49±0.16 ng/ml to 1.74±0.35 ng/ml (P < 0.01). Small decreases in plasma calcium occurred at 0.8 Amol/min epinephrine, but the plasma magnesium remained unchanged. However, when the plasma calcium was lowered with ethylene glycol bis (3-aminoethyl ether) -N, N'-tetraacetic acid (EGTA), a much more pronounced lowering of the plasma calcium was required to produce comparable increases of the plasma iPTH concentrations than when epinephrine was infused. It appears that epinephrine has a direct effect on the release of iPTH from the parathyroid glands.Simultaneous infusions of calcium and epinephrine suppressed the stimulation by epinephrine. This points towards a common mechanism of the regulation of parathyroid hormone secretion caused by decreases in the extracellular calcium concentration and/or alterations in

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“…We recently described the preparation of viable dispersed bovine parathyroid cells which retain many of the morphologic and functional properties recognized physiologically (12). We now show that this cell preparation contains a dopamine receptor that is unequivocally differentiated from the ,B-adrenergic receptor previously identified in this tissue (13)(14)(15)(16). Alterations in cellular cAMP correlate directly with changes in parathyroid hormone (PTH) release, the biologic consequence of increased cAMP in this cell type.…”

mentioning

confidence: 66%

“…Earlier reports that dibutyryl cAMP or aminophylline cause secretion of PTH (15) indicate that cAMP generated in parathyroid cells mediates PTH release in response to dopamine as well as other potential or known secretogogues. In the current experiments, the specificity of the dopamine effect on cAMP and secretion was substantiated further by results with stereospecific (a-versus f,-flupenthixol) inhibition of dopaminergic-receptor interaction.…”

Section: Discussionmentioning

confidence: 99%

Dopaminergic stimulation of cyclic AMP accumulation and parathyroid hormone release from dispersed bovine parathyroid cells

Brown

Carroll

Aurbach

1977

Proc. Natl. Acad. Sci. U.S.A.

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The effects of dopaminergic agonists and antagonists have been studied in dispersed bovine parathyroid cells. Dopaminergic agonists caused a transient 20-to 40-fold increase in cellular cyclic AMP and a 2-to 3fold increase in parathyroid hormone release. Dose-response relationships were similar for cyclic AMP accumulation and hormone release, whether studied by increasing agonist concentration or by increasing concentration of antagonist with constant agonist. The effects on the dopamine receptor could be differentiated from those of the previously characterized f3-adrenergic receptor by specific inhibitors. These results appear to represent proof with a homogeneous cell population that dopaminergic receptors linked to adenylate cyclase can regulate a secretory process mediated by cyclic AMP. This system should be useful in further studies on In most of these studies, preparations from heterogeneous cell populations represented by whole organs, tissue slices, homogenates, or membrane fractions had been used, and functional capacity of the cells had not been determined. Thus, it has been difficult to correlate alterations in biological function directly with changes in cAMP, the presumed intracellular mediator of these effects. We recently described the preparation of viable dispersed bovine parathyroid cells which retain many of the morphologic and functional properties recognized physiologically (12). We now show that this cell preparation contains a dopamine receptor that is unequivocally differentiated from the ,B-adrenergic receptor previously identified in this tissue (13)(14)(15)(16). Alterations in cellular cAMP correlate directly with changes in parathyroid hormone (PTH) release, the biologic consequence of increased cAMP in this cell type. Dispersed bovine parathyroid cells thus provide a useful model for studying the interaction of dopaminergic agonists and antagonists with target tissues. MATERIALS AND METHODSDispersed bovine parathyroid cells were prepared as described (12) by digestion with collagenase and DNase. Incubations were carried out in 20-ml polypropylene scintillation vials (Beckman) in a 370 metabolic shaker (Dubnoff-Precision Scientific Instruments); the medium was Eagle's medium number 2 (bicarbonate deleted) supplemented with 0.02 M N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (Hepes) (pH 7.47), 0.5 mM MgSO4, variable CaCl2 as indicated, and 0.2% heatinactivated bovine serum albumin ("standard medium"). Agonists and antagonists were added directly to the cell suspension (100,000-400,000 cells per ml). In time-course experiments, separate vials were used for each time point.Medium was separated from cells in 400-,g Microfuge tubes (Beckman) and assayed for PTH with a guinea pig anti-bovine-PTH antiserum (12). cAMP was extracted with 5% (wt/vol) perchloric acid, neutralized with potassium bicarbonate, acetylated, and determined by radioimmunoassay with a modification of the method of Harper and Brooker (17). In several experiments, intracellular and extracellular cAMP...

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Evidence for a Role of Adenosine 3′, 5′–Monophosphate in Parathyroid Hormone Release

Cited by 98 publications

References 0 publications

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Decrease in serum immunoreactive parathyroid hormone in rats and in parathyroid hormone secretion in vitro by 1,25-dihydroxycholecalciferol.

Acute Parathyroid Hormone Response to Epinephrine In Vivo

Dopaminergic stimulation of cyclic AMP accumulation and parathyroid hormone release from dispersed bovine parathyroid cells

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