Parathyroid gland system

PTH is secreted from the parathyroid glands in response to a low plasma concentration of ionized (free) calcium. PTH immediately causes the transfer of labile calcium stores from bone into the bloodstream. PTH increases rates of dietary calcium absorption by the intestine indirectly via the vitamin D3 system activation of enterocyte activity. Within the kidney, PTH directly stimulates calcium reabsorption and a phosphate diuresis. 

Other Systemic Effects. Rats administered up to 140 mg 4-nitrophenol/kg/day by gavage for 13 weeks showed no significant effects on body weight gain, or on the gross or microscopical appearance of the salivary glands, pituitary, thyroid and parathyroid glands, adrenals, pancreas, and urinary bladder (Hazleton 1989). 

A second member of the parathyroid hormone family, parathyroid hormone-related protein (PTHrP), is quite similar to PTH in amino acid sequence and protein structure. Like PTH, it activates the parathyroid hormone receptor causing increased bone resorption and renal tubular calcium reabsorption. Increased serum concentrations of parathyroid hormone-related protein are the predominant cause of hypercalcemia in cancer patients with solid tumors. This observation led to its discovery and to the elucidation of its many cellular functions in normal tissues. In contrast to PTH, which is expressed only in parathyroid glands, PTHrP is detected in many tissues in fetuses and adults it is found in epithelia, mesenchymal tissues, endocrine glands, and the central nervous system. This protein is also the principal regulator of placental calcium transport to the fetus. 

Fig. 1. The effect on the systemic plasma calcium concentration of hypercalcemic perfusion of a parathyroid gland in a conscious, thyroidectomized sheep, followed by drainage (D) of the perfused parathyroid venous blood from the animal. The vertical lines represent the standard error. [From Care et al. (C6).]...

The earlier evidence for a second parathyroid hormone (calcitonin) cannot be said to have been either satisfactorily established or finally disproved. Conflicting reports on the systemic effects of separate perfusions of thyroid and of parathyroid glands, and on the presence or otherwise of consistent biphasic effects on plasma calcium when extracts of the parathyroid gland are injected, have contributed to the atmosphere of uncertainty. There are, however, some observations that cannot be readily explained solely on the basis of a thyroid origin for the hypocalcemic principle, notably the effects of cross-transfusion of parathyroid venous plasma in the sheep and the impaired tolerance to infused calcium that follows parathyroidectomy without thyroidectomy. 

Care et al. (C9) have demonstrated that perfusion of the isolated goat parathyroid gland with blood containing an elevated magnesium concentration suppresses the secretion of parathormone in a manner similar to perfusion with hypercalcemic blood. Extension of these studies to the perfusion of pig thyroid with hypermagnesemic blood, however, did not affect the systemic plasma calcium level. It was also shown that per-... 

An important contribution to systemic Ca homeostasis comes from the extracellular calcium-sensing receptor (CaR) (Mithal and Brown 2003). The CaR is a G protein-coupled plasma membrane receptor, by which minute variations in [Ca +] are transduced into changes in cellular functions, including proliferative activity. The CaR is expressed not only in the parathyroid gland (Brown et al. 1993), but importantly also on cells of the main calcium-regulating organs, such as bone (Yamaguchi et al. 

It is now clear that the vitamin D endocrine system is a major factor in the control of plasma calcium and the overall calcium economy of terrestial vertebrates The parathyroid glands monitor calcium concentration of the plasma (Fig. 5) and in response to low blood calcium secrete the parathyroid hormone Parathyroid hormone is taken up by the kidney and bone In the kidney, parathyroid hormone stimulates production of 1,25-(OH)2D3 The 1,25 (OH)2D3 then... 

It is obvious that a variety of disorders would result from a disturbance of the vitamin D endocrine system. Fat malabsorption would result in a deficiency of vitamin D giving rise ultimately to osteomalacia or rickets or secondary hyperparathyroidism. A hepatic disorder such as severe cirrhosis, or biliary atresia, may result in malabsorption of vitamin D and defective vitamin D-25-hydroxylation. Dilantin and phenobarbital cause low plasma 25-OH-D levels resulting in rickets and osteomala-cia246) Qf parathyroid glands would cause a severe hypocalcemia and tetany. 

The more classical Itinehoii of parathyroid hormone is concerned with its control of the maintenance of constant circulating calcium levels. Its action is on 11) Ihe kidney, where it increases the phosphate in the urine. (2) the skeletal system, where it causes calcium resorplion from bone, and t3l the digestive system, where it accelerates (stimulates) calcium absorption into the hitskI The hormone and gland exhibit characteristics of feedback control when the concentration of calcium tons in the blood falls, the secretion of the hormone increases, and when their concentration rises, the secretion of hormone decreases... 

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