The calcemic and phosphaturic effects of parathyroid hormone in the normal and uremic dog

Kaplan, Michael A.; Canterbury, Janet M.; Gavellas, George; Jaffe, David; Bourgoignie, Jacques J.; Reiss, Eric; Bricker, Neal S.

doi:10.1016/0026-0495(78)90264-0

Cited by 21 publications

(13 citation statements)

References 14 publications

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“…The mean iPTH value was 561+54 ,uleq/ml (normal, < 100 ,uleq/ml) for all seven dogs. HPTH is a consistent finding in chronically uremic dogs (4,5,8,9,14,15). After 1 wk of cimetidine administration, the iPTH values fell in all five treated dogs by 12±4…”

Section: Resultssupporting

confidence: 65%

“…The numbers at each point correspond to the dogs in Table I. phate intake. Elevated concentrations of circulating iPTH have been previously demonstrated in chronically uremic man and dog (4,5,8,9,15,17,18). This elevation reflects both an increased rate of secretion of PTH and an accumulation ofmetabolites due to delayed excretion (19).…”

Section: Discussionmentioning

confidence: 92%

“…Reduction ofiPTH was evident despite the persistence of those factors that led to secondary hyperparathyroidism, i.e., a decrease in renal function and maintenance of a "normal" phos- Table I. 2.mr cimetidine-treated dogs is compared with the two cRntrol uremic dogs and an additional eight uremic and eight normal dogs described previously (5). The numbers at each point correspond to the dogs in Table I. phate intake.…”

Section: Discussionmentioning

confidence: 99%

“…For this reason, the prevention and treatment of uremic hyperparathyroidism (HPTH)l remains an area of active investigation (3)(4)(5). We recently reported that cimetidine, a histamine H2 antagonist, decreased circulating concentrations of immunoreactive parathyroid hormone (iPTH) by 75% in a group of hemodialysis patients without associated changes in serum ionized calcium or phosphorus concentrations (6).…”

mentioning

confidence: 99%

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Reversal of Secondary Hyperparathyroidism by Cimetidine in Chronically Uremic Dogs

Jacob¹,

Canterbury²,

Gavellas³

et al. 1981

J. Clin. Invest.

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A B S T R A C T Chronic cimetidine therapy has been shown to suppress circulating concentrations of immunoreactive parathyroid hormone (iPTH) in hemodialysis patients. To evaluate the long-term metabolic effects of cimetidine treatment, we studied seven chronically uremic dogs for 20 wk. The dogs were studied under metabolic conditions before, during, and after cimetidine therapy. iPTH fell progressively in the five treated dogs from 536±70,leq/ml (mean±SE) (nl < 100 ,uleq/ml) before treatment to 291±25 ,leq/ml at 12 wk (P < 0.001) and 157±32 u.leq/ml at 20 wk (P < 0.001). The control dogs showed no consistent change in iPTH. The fall in iPTH was not associated with a change in serum ionized calcium. However, serum phosphorus decreased from 5.7±0.9 mg/dl to 3.4±0.2 mg/dl by the 20th wk (P < 0.05). By contrast, the serum concentration of 1,25-dihydroxycholecalciferol increased in all treated dogs from 33.4±4.3 pg0ml to 51.8±2.4 pg/ml during treatment (P < 0.01). Calcium balance was negative in all seven dogs before cimetidine (-347±84 mg/72 h) and remained so in the control dogs; it became positive in the five treated dogs after 12 wk (1,141±409 mg/72 h) (P < 0.05). Phosphorus balance, 24-h fractional phosphate excretion, and creatinine clearance remained unchanged. Pooled samples of serum obtained during the control and 20th wk of therapy were fractionated by gel filtration and the eluates assayed for immunoreactivity. The decrease in iPTH was associated with a decrease in all the immunoreactive species, indicating suppression of parathyroid gland secretion.These observations indicate that cimetidine suppressed circulating concentration ofbiologically active This work presented in part at the Thirty-seventh Annual

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Section: Resultssupporting

confidence: 65%

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Reversal of Secondary Hyperparathyroidism by Cimetidine in Chronically Uremic Dogs

Jacob¹,

Canterbury²,

Gavellas³

et al. 1981

J. Clin. Invest.

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“…Although these findings may be interpreted as being consistent with prior saturation of parathyroid hormone receptors in muscle by the high levels of circulating parathyroid hormone in chronic uremia (46,47), alternative interpretations are also possible such as a complete desensitization or loss of hormone responsiveness or potentially altered cation pools and channels owing to the hypocalcemia and hyperphosphatemia also associated with chronic uremia (53,54).…”

Section: Discussionmentioning

confidence: 80%

Effects of Parathyroid Hormone on Skeletal Muscle Protein and Amino Acid Metabolism in the Rat

Garber¹

1983

J. Clin. Invest.

127

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A B S T R A C T Because prominent skeletal muscle dysfunction and muscle wasting are seen in both chronic uremia and in primary hyperparathyroidism, and because markedly elevated parathyroid hormone levels occur in both disorders, potential effects of parathyroid hormone on skeletal muscle protein, amino acid, and cyclic nucleotide metabolism were studied in vitro using isolated intact rat epitrochlearis skeletal muscle preparations. Intact bovine parathyroid hormone and the synthetic 1-34 fragment of this hormone stimulated the release of alanine and glutamine from muscle of control but not from chronically uremic animals. This stimulation was dependent upon the concentration of parathyroid hormone added: At 105 ng/ml parathyroid hormone increased alanine release 84% and glutamine release 75%. Intracellular levels of alanine and glutamine were not altered by parathyroid hormone. Increasing concentrations of the 1-34 polypeptide decreased [3HJleucine incorporation into protein of muscles from both control and uremic animals. Using muscles from animals given a pulse-chase label of [guanido-14C]arginine in vivo, parathyroid hormone increased the rate of loss of 14C label from acid-precipitable protein during incubation and correspondingly increased the rate of appearance of this label in the incubation media. Parathyroid hormone increased muscle cAMP levels by 140% and cGMP levels by 185%, but had no effect on skeletal muscle cyclic nucleotide phosphodiesterase activities as assayed in vitro. Adenylyl cyclase activity in membrane preparations from control but not uremic rats was stimulated by parathyroid hormone in a concentration-dependent fashion. However, no stimulation of guanylyl cyclase activity was noted by parathyroid hormone, although stimulation by sodium azide was present. Incubation of muscles with added parathyroid hormone produced a diminished responsiveness towards epinephrine or

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Phosphate transport in the kidney

Bonjour¹,

Caverzasio

1984

Reviews of Physiology, Biochemistry and Pharmacology

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The calcemic and phosphaturic effects of parathyroid hormone in the normal and uremic dog

Cited by 21 publications

References 14 publications

Reversal of Secondary Hyperparathyroidism by Cimetidine in Chronically Uremic Dogs

Reversal of Secondary Hyperparathyroidism by Cimetidine in Chronically Uremic Dogs

Effects of Parathyroid Hormone on Skeletal Muscle Protein and Amino Acid Metabolism in the Rat

Phosphate transport in the kidney

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