Plasma calcium level parathyroid gland

The final mechanism of action of PTH involves the activation of vitamin D3 through the stimulation of la-hydroxylase in the kidney. In the gastrointestinal tract, vitamin D3 is essential for the absorption of calcium. Enhanced absorption of calcium from dietary sources serves to further increase the concentration of calcium in the blood. Many foods, in particular, dairy products, which are rich in calcium, are fortified with vitamin D. The release of PTH from the parathyroid glands is regulated by plasma calcium levels through negative feedback. A decrease in the level of calcium in the blood stimulates the secretion of PTH and an increase in the calcium level in the blood inhibits it. 

The primary factor regulating PTH release is the level of calcium in the bloodstream.42 Parathyroid gland cells appear to act as calcium sensors that monitor circulating calcium levels. As circulating calcium levels fall below a certain point, PTH secretion is increased. Conversely, elevated plasma calcium titers inhibit PTH secretion. The ability of PTH to control plasma calcium levels and regulate bone mineral metabolism is discussed in more detail in Chapter 31... 

PTH is a polypeptide hormone that is synthesized within the cells of the parathyroid glands. The primary factor controlling the release of PTH is the amount of calcium in the bloodstream.36 A calciumsensing receptor is located on the outer surface of the parathyroid cell membrane, and this receptor monitors plasma calcium levels.11,88 A decrease in plasma calcium activates this receptor and causes increased release of PTH. As blood calcium levels increase, the receptor is inhibited, and PTH release is reduced. 

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-... 

The polypeptide parathormone is released from the parathyroid glands when plasma Ca + level falls. It stimulates osteoclasts to increase bone resorption in the kidneys, it promotes calcium reabsorption, while phosphate excretion is enhanced. As blood phosphate concentration diminishes, the tendency of calcium to precipitate as bone mineral decreases. By stimulating the formation of vit D hormone, parathormone has an indirect effect on the enteral uptake of Ca + and phosphate. In parathormone deficiency, vitamin D can be used as a substitute that unlike parathormone, is effective orally. 

Q2 The hormones that are normally involved in the control of calcium balance are parathyroid hormone (PTH) from the parathyroid gland calcitonin, which is secreted by the thyroid gland and 1,25-dihydroxycholecalciferol (1,25-DHCC, or calcitriol), which is produced in the kidneys. Calcitonin reduces the level of plasma calcium by attenuating its release from bone and by increasing its excretion. The PTH and 1,25-DHCC increase the level of plasma calcium by two mechanisms (1) a combination of an increase in calcium absorption by the gut and an increase in the release of calcium from bone and (2) a reduction in both bone formation and calcium excretion. The three hormones act together to maintain the physiological level of calcium and normal bone turnover. Over 95% of body calcium is located in bone as hydroxyapatite. 

Calcitonin is a 32-amino-acid polypeptide hormone that was hrst purihed in 1962 by Copp and Cheney (121). It was originally thought as a product from parathyroid glands, but later it was discovered to be made by the C cells of the thyroid gland. Calcitonin participates in calcium and phosphorus metabolism, lowers plasma calcium and phosphate levels, and it has been used as a drug for bone and mineral disorders for a long time. 

To summarize the overall scenario, as extracellular calcium ion levels decline, the parathyroid gland increases its release of parathyroid hormone, thus increasing plasma Ca and restoring it to proper levels. Most cdJs of the body contain some elements of the preceding signaling scheme, as revealed at a later point in this section,... 

The free calcium ions in blood and extracellular fluid are critical for building and maintaining an adequate bone mass, and also for preventing excessive calcification. The sensor that regulates the free calcium ion concentration of plasma is within the parathyroid glands, where it controls the secretion of parathormone (PTH). This 84 amino acid peptide is split from a large, precursor protein and retained in secretory vesicles. If the concentration of free calcium ions drops below a critical level in blood plasma, the gland is activated to secrete PTH into the bloodstream. 

It is g erally assumed that it is the concentration of ionic calcium in the extracellular fluid which the parathyroid glands control by this action on the skeleton and that the variations in total plasma calcium are strictly proportional. However, Freeman and Breen (Fll) have shown that parathyroidectomy is followed by a rise in the proportion of protein-boimd calcium and that this can be reduced by injection of the hormone. This accords with the observations of Lloyd and Rose in hyperparathyroidism (L6 see Section 4.2) and with the clinical observation that hypo-parathyroid patients may develop tetany at surprisingly high levels of total plasma calcium. The effects of Ae hormone on add-base balance may be concerned in this phenomenon since acidemia reduces the proportion of protein-bound calcium. 

The secretion of the parathyroid glands is probably controUed by die concentration of ionic calcium concentration in the tissue fluid. Artificial elevation of plasma calcium suppresses the parathyroids (H12, K5, N5), and parathyroid size varies inversely with the level of plasma calcium (HI, S6). Part and Luckhardt (P3) demonstrated an increase in parathyroid hormone secretion in response to the perfusion of parathyroid glands with fluids of low calcium concentration. Talmage s osteoclast count, which is believed to measure parathyroid activity, rises in response to rapid removal of calcium from the extracellular fluid of intact rats (T2). The precise ionic calcium levels which stimulate and suppress the parathyroids are not known, but calcium infusions suggest that parathyroid suppression occurs when total plasma calcium rises above about 11 mg/100 ml. Stimulation probably occurs when the concentration falls below about 9 mg/100 ml. 

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