The relationship between the actions of vitamin D, parathyroid hormone and calcitonin
The effect of PTH and CT upon hydroxyproline and electrolyte excretion, plasma calcium and phosphate, calcium balance, and the excretion of radiocalcium was examined in vitamin D-deficient thyroparathyroidectomized rats. The results were compared to those obtained in D-fed animals. An increase in urinary hydroxyproline, which persisted for many hours, occurred in D-deficient animals approximately 30 h after thyroparathroidectomy, but was not seen in D-fed animals. It was suppressed by high calcium infusion. Infusion of PTH or CT increased the hydroxyprolinuria even further in D-deficient animls. PTH increased hydroxyprolinuria in D-fed animals, but CT caused a significant decrease. In the D-deficient animals both PTH and CT caused a decrease in urinary calcium excretion, and an increase of the already positive calcium balance. In D-fed animals CT had similar effects, but PTH caused a significant increase in calcium excretion and a negative calcium balance. Young animals injected with45Ca while on a D-deficient diet were studied 3 weeks later at a time when they had developed D-deficiency. When these animals were thyroparathyroidectomized and maintained on a constant glucose and electrolyte perfusion, the excretion of calcium was relatively constant and the specific activity of urnary calcium declined only slightly over a 28 h period. When PTH was given, both total and radioactive calcium excretion diminished initially, leading to a significant decrease in specific activity. The specific activity declined for the first 3 h of hormone infusion, then rose gradually and became greater than normal during the last 4 h of hormone infusion. When CT was given with PTH, total calcium excretion fell and remained below the control rate throughout the experiment. Specific activity rose markedly during the first 2 h, then fell rapidly to values below the control levels for the remainder of the experiment.
Article: Azotaemic rend osteodystrophyBritish Medical Bulletin 02/1957; 13(1):57-60. DOI:10.1016/S0300-595X(72)80060-4 · 3.66 Impact Factor
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ABSTRACT: The cellular control systems which form the underlying basis for mammalian calcium homeostasis are nearly identical to the cellular control systems involved in the activation of secretion in the fly salivary gland by the hormone serotonin. This similarity attests to the correctness of the original premise that extracellular calcium homeostasis in the mammalian organism is achieved by an adaptation and extension of those much more ancient systems developed early in evolution to maintain intracellular calcium homeostasis. The unique features of mammalian extracellular calcium homeostasis thus lie not in the development of new or unique cellular control systems, but in the highly selective manner in which a common biochemical control device is regulated by specific extracellular messengers in the highly differentiated cells of the mammalian organism. In addition, this view of the control of both cellular and extracellular calcium homeostasis emphasises that the concentration of this ion is of critical importance in regulating both key extra and intracellular, or more correctly, cytosolic systems, and that changes in its concentration within the cell cytosol are an important means of regulating cell function. (Journal received: January, 1975.)Clinics in Endocrinology and Metabolism 03/1972; 1(1). DOI:10.1016/S0300-595X(72)80048-3
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ABSTRACT: The presence of hyperparathyroidism in early renal failure was first suggested by the data of Friis, Hahnemann and Weeke  which showed that serum phosphate was lower in patients with small decreases in glomerular filtration rate (GFR) (< 40 ml/min) than in a control group of normals. Also, Popovtzer et al  showed that the urinary calcium excretion was lower than normal in a similar group of patients. This hyperparathyroidism was demonstrated directly by Reiss, Canterbury and Egdahl , who found significantly increased serum immunoreactive parathyroid hormone (iPTH) levels at GFR values as high as 70 to 80 ml/min. Data from my laboratory regarding this point are shown in Fig. 1. But our data differ from those of Reiss, Canterbury and Egdahl  in that significant increases in serum iPTH were first noted at inulin clearance values below 40 ml/min. This difference may be related in some way to the immunoheterogeneity of serum iPTH, which will be discussed later in the section on the radioimmunoassay of PTH. The important points to be derived from these studies, however, are that secondary hyperparathyroidism begins early and that its severity is related, in general, to the degree of renal functional impairment, as originally suggested by Berson and Yalow  who were the first to demonstrate that serum iPTH was increased in renal failure.Kidney International 09/1973; 4(2):89-95. DOI:10.1038/ki.1973.87 · 8.56 Impact Factor
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