The effect of parathyroid hormone on adenyl cyclase in rat kidney

Douša, Tomáš; Rychlík, Ivan

doi:10.1016/0304-4165(68)90309-7

Cited by 50 publications

(11 citation statements)

References 2 publications

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“…It is considered unlikely that fluoride ion increases cyclic AMP accumulation simply by preserving substrate because the effect of this ion can still be observed when an ATP regenerating system is used. However, in most studies in which an ATP regenerating system was used, it was not established that the ATP concentration was maintained throughout the duration of the experiment (Rabinowitz, Desalles, Meisler & Lorand, 1965;Streeto & Reddy, 1967;Dousa & Rychlik, 1968).…”

Section: Introductionmentioning

confidence: 99%

The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by NaF

Katz

Tenenhouse

1973

British J Pharmacology

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Sunmmary1. A method for measuring the rate of production of "IC-labelled adenine nucleotides, including cyclic adenosine 3',5'monophosphate (cyclic AMP), from ["IC]-adenosinetriphosphate (ATP) was developed and used to study the effects of ATP, adenosine diphosphate (ADP) and adenosine 5'-monophosphate (AMP) on the rate of accumulation of cyclic AMP in cell-free preparations of adenyl cyclase from rat brain. 2. The mechanism by which NaF increases cyclic AMP accumulation was studied by comparing its effect on adenine nucleotide metabolism with that of an ATP regenerating system.3. ADP and ATP are potent inhibitors of phosphodiesterase (PDE) and it is the sum of the concentrations of these two nucleotides which controlled the rate of destruction of cyclic AMP. The effect of these nucleotides was significant even in the presence of 6-7 mm theophylline; theophylline itself inhibited PDE only 50-60%. 4. Fluoride ion had no direct effect on PDE but it inhibited the rate of hydrolysis of ADP and ATP and thus indirectly inhibited PDE. The effect of fluoride ion on cyclic AMP accumulation can be explained, at least in part, by this indirect inhibition of PDE.5. Studies on a more purified preparation of adenyl cyclase clearly demonstrated a direct action of NaF on adenyl cyclase.

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Section: Introductionmentioning

confidence: 99%

The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by NaF

Katz

Tenenhouse

1973

British J Pharmacology

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“…This hypothesis was based on the observation that patients with this disorder did not show the characteristic phosphaturic response to parathyroid extract. The recent findings that the mechanism of action of parathyroid hormone is mediated through activation of adenyl cyclase in kidney (2)(3)(4) and bone (5) suggested further investigation into the nature of the biochemical defect in pseudohypoparathyroidism. Parathyroid hormone affects specifically the membrane-bound enzyme adenyl cyclase in the renal cortex (3) and in bone (5) causing a marked increase in the concentration of adenosine 3',5'-monophosphate (3',5'-AMP) in these tissues (6,71).…”

Section: Introductionmentioning

confidence: 99%

Pseudohypoparathyroidism: defective excretion of 3′,5′-AMP in response to parathyroid hormone

Chase¹,

Melson²,

Aurbach³

1969

J. Clin. Invest.

467

158

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A B S T R A C T Urinary excretion of cyclic adenosine 3',5'-monophosphate (3',5'-AMP) was tested in normal subjects and patients with pseudohypoparathyroidism, idiopathic hypoparathyroidism, surgical hypoparathyroidism, and pseudopseudohypoparathyroidism under basal conditions and after a 15 min infusion of purified parathyroid hormone. Basal excretion of the nucleotide was less than normal in the patients with hypocalcemic disorders and greater than normal in pseudopseudohypoparathyroidism. Parathyroid hormone caused a marked increase in excretion of 3',5'-AMP in all subjects except those with pseudohypoparathyroidism; nine patients with this disorder did not respond to the hormone and four showed a markedly deficient response. Radioimmunoassay showed that parathyroid hormone circulated in increased amounts in plasma from patients with pseudohypoparathyroidism and became undetectable when serum calcium was increased above 12 mg/100 ml. Suppression of parathyroid hormone secretion by induction of hypercalcemia did not alter the deficient response to exogenous hormone. The results indicate that: (a) parathyroid hormone circulates in abnormally high concentrations in pseudohypoparathyroidism and secretion of the hormone responds normally to physiological control by calcium; (b) testing urinary excretion of 3',5'-AMP in response to infusion of purified parathyroid hormone appears to-be an accurate and sensitive index for establishing the diagnosis of pseudohypoparathyroidism; and (c) the metabolic defect of the disorder can be accounted for by a lack of or defective form of parathyroid hormone-sensitive adenyl cyclase in bone and kidney.

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“…DISCUSSION There are at least three lines of evidence which support the view that the effects of PTH on bone and kidney are mediated through the adenyl cyclase system. First, PTH activates adenyl cyclase in both rat kidney (7,8) and rat skeletal tissue (9) and increases urinary cyclic AMP in man (4,10) and laboratory animals (11). Second, PTH stimulates the accumulation of cyclic AMP in fetal rat calvaria (12 (17).…”

Section: Introductionmentioning

confidence: 99%

Effects of Dibutyryl Cyclic Adenosine 3′,5′-Monophosphate and Parathyroid Extract on Calcium and Phosphorus Metabolism in Hypoparathyroidism and Pseudohypoparathyroidism

Bell¹,

Avery²,

Sinha³

et al. 1972

J. Clin. Invest.

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A B S T R A C T It has been proposed previously that the metabolic defect in pseudohypoparathyroidism which accounts for parathyroid hormone unresponsiveness is an absence or abnormal form of the adenyl cyclase system in kidney and presumably in bone. To determine whether there is an associated defect in the response mechanism to cyclic adenosine 3',5'-monophosphate (cyclic AMP), the effects of parathyroid extract (PTE), and dibutyryl cyclic AMP were compared in patients with either surgical hypoparathyroidism or pseudohypoparathyroidism. PTE and dibutyryl cyclic AMP both increased serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in patients with hypoparathyroidism. PTE also increased urinary cyclic AMP in these patients. PTE increased serum and urinary calcium and urinary phosphorus but did not alter serum phosphorus or urinary cyclic AMP in the patients with pseudohypoparathyroidism. Dibutyryl cyclic AMP increased the serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in all the patients with pseudohypoparathyroidism. The results indicate that (a) dibutyryl cyclic AMP can reproduce the effects of parathyroid hormone on calcium and phosphorus metabolism in man, (b) the response mechanism to cyclic AMP appears to be intact in pseudohypoparathyroidism, and (c) PTE apparently produces some of its characteristic effects on calcium and phosphorus metabolism in pseudohypoparathyroidism in the absence of an increase in urinary cyclic AMP.

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The effect of parathyroid hormone on adenyl cyclase in rat kidney

Cited by 50 publications

References 2 publications

The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by NaF

The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by NaF

Pseudohypoparathyroidism: defective excretion of 3′,5′-AMP in response to parathyroid hormone

Effects of Dibutyryl Cyclic Adenosine 3′,5′-Monophosphate and Parathyroid Extract on Calcium and Phosphorus Metabolism in Hypoparathyroidism and Pseudohypoparathyroidism

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