Urinary cyclic AMP response to bovine parathyroid hormone during treatment with neuroleptics

1987 ◽  
Vol 2 (2) ◽  
pp. 105-107 ◽  
Author(s):  
Derek G. Waller ◽  
Janet D. M. Albano ◽  
J. Guyedwards
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Urinary Cyclic Amp ◽  
Bovine Parathyroid Hormone

Cyclic AMP Responses to Parathyroid Hormone and Glucagon during Lithium Treatment

1984 ◽  
Vol 66 (5) ◽  
pp. 557-559 ◽  
Author(s):  
D. G. Waller ◽  
J. D. M. Albano ◽  
J. G. B. Millar ◽  
A. Polak
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Intravenous Injection ◽  
Lithium Treatment ◽  
Endocrine Dysfunction ◽  
Urinary Cyclic Amp ◽  
Urine Concentrating Ability ◽  
Bovine Parathyroid Hormone

1. Inhibition of adenylate cyclase has been proposed as a mechanism for hypothyroidism and nephrogenic diabetes insipidus occurring during lithium treatment, but these disorders are rarely found in the same patients. 2. We have measured plasma levels of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) after an intravenous injection of glucagon in eight patients receiving long term lithium treatment and in six control subjects. Urinary cyclic AMP levels after an intravenous injection of bovine parathyroid hormone (PTH) were also measured in the patients. 3. The plasma cyclic AMP response to glucagon in the patient group was significantly lower than that of the controls. No correlation was demonstrated between the plasma cyclic AMP response after glucagon and the urinary cyclic AMP response after PTH. 4. We have previously shown that impairment of the response to PTH correlates with reduced urine concentrating ability during lithium treatment. In contrast, there was no correlation between the responses to PTH and glucagon in individual patients. These results are consistent with the hypothesis that inhibition of adenylate cyclase is an important factor in lithium-induced endocrine dysfunction.

Impairment of Cyclic AMP Response to Bovine Parathyroid Hormone in Patients on Chronic Lithium Therapy with Diminished Renal Urine-Concentrating Ability

1983 ◽  
Vol 64 (6) ◽  
pp. 623-627 ◽  
Author(s):  
D. G. Waller ◽  
J. D. M. Albano ◽  
J. G. B. Millar ◽  
A. Polak
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Intravenous Injection ◽  
Lithium Treatment ◽  
Urine Osmolality ◽  
Control Subjects ◽  
Urinary Cyclic Amp ◽  
Urine Concentrating Ability ◽  
Bovine Parathyroid Hormone

1. Urinary and plasma levels of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) after an intravenous injection of bovine parathyroid hormone (PTH) were measured in 12 patients on long-term lithium treatment and in nine control subjects. The maximum urine osmolality (Umax.) after an intravenous injection of desamino-d-arginine vasopressin (DDAVP) was also measured. 2. in all the control subjects and six of the patients, the Umax. after DDAVP exceeded 700 mosmol/kg. The cyclic AMP responses in these two groups did not differ significantly. 3. in the remaining six patients whose Umax. did not reach 700 mosmol/kg, the cyclic AMP response to PTH was significantly less than that of the controls. 4. A strong correlation was demonstrated in the patients between the urinary cyclic AMP response after PTH and the maximum osmolality after the administration of DDAVP. 5. These observations are consistent with the hypothesis that reduced adenylate cyclase activity contributes to the development of nephrogenic diabetes insipidus in patients on long-term lithium treatment.

Impaired renal response to parathyroid hormone in potassium depletion

1975 ◽  
Vol 228 (1) ◽  
pp. 179-183 ◽  
Author(s):  
N Beck ◽  
BB Davis
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Potassium Depletion ◽  
Dibutyryl Cyclic Amp ◽  
Renal Response ◽  
Proximal Tubular ◽  
Urinary Cyclic Amp

In potassium depletion, a possible alteration of the proximal tubular response to parathyroid hormone (PTH) was evaluated in rat kidney. 1) There were impairments of both phosphaturic and urinary cyclic AMP responses to PTH. The site of the impairment was further investigated by studying the PTH-dependent cycle AMP system in renal cortex. 2) There was a lesser increase of cyclic AMP concentration by PTH in potassium-depleted slices, indicating the lesser urinary cyclic AMP was due to the specific impairment of PTH-dependent cyclic AMP in the kidney. 3). The activation of adenylate cyclase by PTH was impaired , but phosphodiesterase activity was not affected by potassium depletion, indicating the impairment of cyclic AMP generation was due to inhibition of adenylate cyclase. 4) The phosphaturic response to dibutyryl cyclic AMP infusion was also significantly less in the potassium-depleted animals, indicating the step subsquent to the cyclic AMP generation is also impaired. All above results indicate that, in potassium depletion, the renal response to PTH is impaired, and the impairment is both within the step of cyclic AMP generation and after the cyclic AMP generation.

Calcium-dependent, parathyroid hormone-independent regulation of 1,25-dihydroxyvitamin D

1980 ◽  
Vol 239 (2) ◽  
pp. E119-E124 ◽  
Author(s):  
U. Trechsel ◽  
J. A. Eisman ◽  
J. A. Fischer ◽  
J. P. Bonjour ◽  
H. Fleisch
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Calcium Intake ◽  
Dietary Calcium ◽  
Dihydroxyvitamin D ◽  
Calcium Dependent ◽  
1,25 Dihydroxyvitamin D ◽  
Urinary Cyclic Amp ◽  
Pth Level

The increase of plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) in response to Ca restriction has been suggested to be essentially mediated by parathyroid hormone (PTH). In this study, we have assessed the influence of variations in calcium intake on plasma 1,25(OH)2D in pair-fed sham-operated (sham) and in hypocalcemic hypoparathyroid rats after thyroparathyroidectomy (TPTX). In sham rats, plasma 1,25(OH)2D increased from 189 +/- 16 to 486 +/- 41 pM when dietary calcium was inreased from 1.2% Ca to 0.2% Ca. This increase was associated with an increase in plasma PTH level. In TPTX rats, plasma 1,25(OH)2D increased from 112 +/- 9 to 332 +/- 36 pM when dietary calcium was decreased. In this case, the increase was not associated with a rise in plasma PTH level nor with an increase in urinary cyclic AMP. When TPTX rats were infused chronically with PTH (60 U/day), plasma 1,25(OH)2D was 62 +/- 9 pM when the 1.2% Ca diet was given and 281 +/- 45 pM with the 0.2% Ca diet. These reults confirm that the thyroparathyroid glands influence plasma 1,25(OH)2D but they also provide evidence for a PTH-independent response of plasma 1,25(OH)2D to Ca restriction.

NEWBORN URINARY CYCLIC AMP AND DEVELOPMENTAL RENAL RESPONSIVENESS TO PARATHYROID HORMONE

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 14-23 ◽  
Author(s):  
Louie G. Linarelli ◽  
John Bobik ◽  
Caroline Bobik
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Adenosine Monophosphate ◽  
Fourfold Increase ◽  
Before And After ◽  
Renal Action ◽  
Proximal Tubular ◽  
Insignificant Difference ◽  
Urinary Cyclic Amp ◽  
Renal Proximal Tubular

Since the renal action of parathyroid hormone is known to be mediated via 3',5'-adenosine monophosphate (cyclic AMP), urinary cyclic AMP studies were used to determine proximal tubular maturation. Ten formula fed full-term male infants showed a thirty- to sixtyfold increase in phosphate clearance and excretion with a three- to fourfold increase in urinary cyclic AMP comparing their first and third day 24-hour urines (2.37 ± 0.41 to 6.93 ± 0.96 Nm/mg creatinine M. ± S.E.M. first and third days respectively). Seven breast-fed infants showed cyclic AMP excretion of 3.6 ± 0.3 S.E.M. and 6.5 ± 0.3 S.E.M. on Day 1 and Day 3 respectively, showing an insignificant difference to the formula-fed infants. An additional 10 formula-fed infants 5 to 10 days of age excreted 7.0 ± 0.9 S.E.M. Nm/mg of creatinine which is comparable to the 3 to 4 days of age group. The threefold increase in cyclic AMP after the first day of life may possibly reflect increasing parathyroid renal responsiveness. One- and 3-day-old infants and adults were given a 1-hour parathyroid (PTH) infusion (5 U/kg/hr) with measurement of urinary cyclic AMP in time periods before and after the infusions. Peak increases in responses from baseline of cyclic AMP were 1.64 ± 0.34, 7.1 ± 1.5, and 36.0 ± 0.73 Nm/mg of creatinine M. ± range on first day, third day, and in adults respectively with similar relationships of increasing phosphate excretion. Thus, there is most likely a maturational renal proximal tubular responsiveness to PTH on the cellular cyclic AMP level.

Control of Renal Tubular Phosphate Reabsorption by Parathyroid Hormone in Man

1977 ◽  
Vol 53 (5) ◽  
pp. 431-438
Author(s):  
D. A. Walker ◽  
S. Joyce Davies ◽  
K. Siddle ◽  
J. S. Woodhead
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Primary Hyperparathyroidism ◽  
Normal Subjects ◽  
Vitamin D Metabolism ◽  
Phosphate Reabsorption ◽  
Important Regulator ◽  
Urinary Cyclic Amp ◽  
Renal Tubular

1. The maximum tubular reabsorption capacity for phosphate relative to glomerular filtration rate (Tm,P/GFR) was found to range from 0·8 to 1·5 mmol/l in 32 normal fasting subjects. In 14 patients with primary hyperparathyroidism and five patients with hyperparathyroidism secondary to vitamin D deficiency or malabsorption values ranged from 0·2 to 0·8 mmol/l. 2. Plasma parathyroid hormone concentrations measured by an immunoradiometric technique ranged from <0·15 to 0·9 ng/ml in the normal subjects and from 0·5 to 10 ng/ml in the patients with hyperparathyroidism. There was no correlation, however, between plasma parathyroid hormone and Tm,P/GFR in either normal or abnormal groups. 3. Plasma parathyroid hormone was lower in 11 out of 13 patients with primary hyperparathyroidism 3 or 4 weeks after tumour removal than immediately before the operation. In all cases there was a rise in Tm,P/GFR, though not all values were normalized. 4. Changes in plasma parathyroid hormone, Tm,P/GFR and plasma and urinary cyclic AMP concentrations were measured during infusion of bovine parathyroid hormone into normal fasting subjects. Phosphate reabsorption fell markedly in response to low doses of parathyroid hormone (0·5 i.u. h−1 kg−1), higher doses (4 i.u. h−1 kg−1) producing little additional change in Tm,P/GFR despite large changes in cyclic AMP excretion. At the highest doses used (8 i.u. h−1 kg−1) apparent saturation of the renal adenylate cyclase occurred. During an infusion of hormone, 0·25 i.u. h−1 kg−1 over 3 h, a fall in Tm,P/GFR was recorded at concentrations of immunoreactive parathyroid hormone within the normal range for endogeneous hormone. At such concentrations it was not possible to detect significant changes in either plasma or urine cyclic AMP. 5. It is concluded that parathyroid hormone is an important regulator of renal phosphate handling under normal physiological conditions. Such a regulatory process has been implicated in the control of vitamin D metabolism.

Reversible Resistance to the Renal Action of Parathyroid Hormone in Man

1976 ◽  
Vol 51 (1) ◽  
pp. 59-69 ◽  
Author(s):  
S. Tomlinson ◽  
G. N. Hendy ◽  
D. M. Pemberton ◽  
J. L. H. O'Riordan
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Intravenous Injection ◽  
Normal Subjects ◽  
Standard Test ◽  
Initial Increase ◽  
Partial Recovery ◽  
Amino Terminal ◽  
Receptor Sites ◽  
Bovine Parathyroid Hormone

1. Normal subjects showed a highly reproducible, rapid increase in plasma adenosine 3′:5′-cyclic monophosphate (cyclic AMP) after an intravenous injection of 200 MRC units of highly purified bovine parathyroid hormone. 2. No significant increase in plasma cyclic AMP was observed after administration of bovine parathyroid hormone to patients with severe chronic renal failure. 3. Even when renal function was not impaired, some patients with primary hyperparathyroidism, who had high concentrations of endogenous parathyroid hormone, showed resistance to bovine parathyroid hormone and when this was injected intravenously it caused only a small increase in plasma cyclic AMP. This resistance was reversible since there was marked improvement in the response after parathyroidectomy, when endogenous parathyroid hormone concentration had fallen. 4. It was possible to reproduce this resistance to the hormone by intravenous infusion of bovine parathyroid hormone into normal subjects. When the hormone (1000 MRC units) was infused over 2 h, after an initial increase there was a progressive decline in plasma cyclic AMP concentration and a fall in urinary cyclic AMP excretion. The response to a standard test stimulus (200 MRC units of bovine parathyroid hormone given as a rapid intravenous injection) was examined at intervals after 1000 units of bovine parathyroid hormone had been infused. Initially, the response was severely impaired; at 4 h, partial recovery had occurred and, 24 h after the infusion, recovery of the response was complete. The resistance was therefore reversible. Infusion of the amino-terminal peptide, fragment 1–34, gave the same effect as infusion of intact hormone. Region-specific assays for the hormone were used to show that the concentration of immuno-assayable hormone remained high during the infusions. 5. The mechanism of this reversible resistance to parathyroid hormone remains to be elucidated; it seems unlikely that circulating hormone fragments could account for the prolonged impairment in the responsiveness to the intact hormone. It is possible that alteration in the formation, intracellular degradation or, perhaps, release of cyclic AMP from the cells, is the cause. Changes in the characteristics of the hormone receptor sites might also explain the phenomenon.

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