Endocrine system parathyroid

Calcium is present in three forms e.g., as free calcium ion, bound to plasma protein albumin and in diffusable complexes. The endocrine system, through parathyroid hormone and calcitonin, helps in keeping the concentration of ionized plasma calcium in normal level. Decrease in plasma levels of ionized calcium leads to increased parathyroid hormone secretion. Parathyroid hormone tends to increase plasma calcium level by increasing bone resorption, increasing intestinal absorption and increasing reabsorption of calcium in kidney. Vitamin D acts by stimulating... 

Pig. 5. Diagramatic repiesentation of calcium homeostatic mechanisms involving the vitamin D endocrine system located in the kidney. Note that the calcium sensing organs are the para-thryoid glands (hypocalcemia) and the C-cells of the thyroid (hypercalcemia). Note that the vitamin D hormone acts by itself on the intestine and together with parathyroid hormone in bone and kidney... 

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. 

Endocrine system. Lanthanum binds to the cell surface of parathyroid cells (without entering the cells), but this gives rise to increased Ca permeability resulting in a rise in intracellular Ca (Gylfe, Larsson et al. 1986). Parathyroid hormone (PTH) release from the gland is normally inhibited by Ca but is inhibited by lanthanum to an even greater extent. Incubation of parathyroid cells with pertussis toxin, a G-protein inactivator that blocks inhibition by Ca, does not block the inhibition of PTH release by lanthanum. There may be two cell surface sites that recognize lanthanmn and Ca independently (Fitzpatrick 1990).. 

Endocrine topics not discussed in Chapters 30-34 that are covered elsewhere in the text are as follows gastrointestinal hormones, Chapter 12 eicosanoids, Chapter 18 pancreatic hormones, Chapter 22 parathyroid hormone and vitamin D, Chapter 37 renin-angiotensin system and antidiuretic hormone. Chapters 32 and 39. A list of expanded acronyms appears in Appendix VIIl. 

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. 

Regulation of Secretion Plasma Ca +is the major regulator of PTH secretion hypocalcemia stimulates and hypercalcemia inhibits PTH secretion. Sustained hypocalcemia also induces parathyroid hypertrophy and hyperplasia. Changes in Ca modulate PTH secretion by parathyroid cells via the calcium-sensing receptor (CaSR), a GPCR that couples with G -PLC and G. Occupancy of the CaSR by Ca inhibits PTH secretion thus, the extracellular concentration of Ca is controlled by an endocrine negative-feedback system, the afferent limb of which senses the ambient activity of Ca and the efferent hmb of which releases PTH that then acts to increase Ca. The active vitamin D metabolite calcitriol directly suppresses PTH gene expression. 

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