Sleep shift dissociates the nocturnal peaks of parathyroid hormone (1-84), nephrogenous cyclic adenosine monophosphate, and prolactin in normal men.

1992 ◽  
Vol 75 (1) ◽  
pp. 25-29
Author(s):  
F C Logue ◽  
W D Fraser ◽  
D S O'Reilly ◽  
J Christie ◽  
D A Cameron ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Men

THE CIRCADIAN RHYTHM OF INTACT PARATHYROID HORMONE (1-84) AND NEPHROGENOUS CYCLIC ADENOSINE MONOPHOSPHATE IN NORMAL MEN

1989 ◽  
Vol 121 (1) ◽  
pp. R1-R3 ◽  
Author(s):  
F.C. Logue ◽  
W.D. Fraser ◽  
D.St.J. O'Reilly ◽  
G.H. Beastall
Keyword(s):  
Circadian Rhythm ◽  
Parathyroid Hormone ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Significant Rise ◽  
Optimal Time ◽  
Normal Male ◽  
Intact Parathyroid Hormone ◽  
Normal Men ◽  
Nocturnal Rise

ABSTRACT A pronounced circadian rhythm has been demonstrated for intact parathyroid hormone (1-84) in the serum of normal male adults. The broad nocturnal rise of parathyroid hormone (1-84) secretion appears to be of physiological significance, for it is accompanied by a significant rise in nephrogenous cyclic adenosine monophosphate. The rate of return of parathyroid hormone (1-84) to baseline concentrations varies between individuals, an observation which has implications for the optimal time of sampling for the investigation of possible mild hyperparathyroidism.

Divergent effects of forskolin on 3′,5′ cyclic adenosine monophosphate production and parathyroid hormone secretion

1984 ◽  
Vol 36 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Larry K. Cantley ◽  
Drusilla L. Scott ◽  
Cary W. Cooper ◽  
Darien D. Mahaffee ◽  
George S. Leight ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate

Lithium administration and phosphate excretion

1976 ◽  
Vol 231 (4) ◽  
pp. 1140-1146 ◽  
Author(s):  
JA Arruda ◽  
JM Richardson ◽  
JA Wolfson ◽  
L Nascimento ◽  
DR Rademacher ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Renal Cortex ◽  
Cyclic Adenosine Monophosphate ◽  
Fractional Excretion ◽  
Adenosine Monophosphate ◽  
Adenyl Cyclase ◽  
Phosphate Excretion ◽  
Camp System

The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.

Clinical and laboratory studies of a new immunoradiometric assay of parathyroid hormone-related protein

1993 ◽  
Vol 39 (3) ◽  
pp. 414-419 ◽  
Author(s):  
W D Fraser ◽  
J Robinson ◽  
R Lawton ◽  
B Durham ◽  
S J Gallacher ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Detection Limit ◽  
Limit Of Detection ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Patient Specific ◽  
Immunoradiometric Assay ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein

Abstract Parathyroid hormone-related protein (PTHrP) was measured in plasma by a new immunoradiometric assay (IRMA) from Nichols Institute. The assay is specific for PTHrP and shows excellent parallelism when measuring keratinocyte fluid, samples with high PTHrP content, and PTHrP-supplemented plasma. A precision profile established the assay detection limit at 0.7 pmol/L. PTHrP was unstable in plasma, but the degradation rate was patient-specific. Because delay in separation resulted in loss of PTHrP immunoreactivity, samples were collected into tubes containing protease inhibitors (aprotinin, leupeptin, pepstatin, and EDTA) and separated within 30 min. Among normal subjects, 78% had PTHrP values greater than the detection limit; the reference range established was < 0.7-2.6 pmol/L. Of patients with hypercalcemia associated with malignancy, 46% had PTHrP > 2.6 pmol/L. PTHrP was increased in patients with breast (73%), genitourinary (64%), or lung (46%) malignancy but was rarely above normal in patients with hematological (29%) or gastrointestinal (33%) malignancy. PTHrP and nephrogenous cyclic adenosine monophosphate (NcAMP) were strongly correlated (r = 0.63, P < 0.01) in 37 patients with PTHrP values greater than the detection limit, but 8 patients had PTHrP and parathyroid hormone [PTH(1-84)] values below the limit of detection with inappropriate or increased NcAMP. Five of these eight patients had small cell carcinoma of lung. These patients may have secreted a factor that is not detected by the IRMAs of PTHrP or PTH used in this study but that produces hypercalcemia by means of cAMP-mediated mechanisms.

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