Compensated PTH

I able 16.12. First-order rate constants for the loss of the FTIR band intensity (associated to 2,5-substitutcd thiophene ring) in ammonia compensated PTH(Bp4) during thermal degradation at 80°, 175°, 250° and 400°C in air. Adapted from Synth. Met. 66, 33 (1994), permission of Elsevier Science S.A., Lausanne... 

Parathyroid hormone stimulates bone resorption by increasing the number and activity of osteoclasts. This demineralization process in the bone releases calcium and phosphate into the blood. Although the action of PTH on the bone appears to increase blood phosphate, its action on the kidney, which increases phosphate excretion in the urine, more than compensates for this increase and the net effect is a decrease in serum phosphate. 

Vitamin D is essential for the action of parathormone on osteoclasts whereby bone resorption and a hypercalcaemic response are induced. For this reason parathormone is comparatively inactive in patients with rickets. The mechanism of this synergistic effect is not clear but, since actinomycin D blocks the hypercalcaemic activity of vitamin D, it may be that the vitamin induces the formation of a calcium-binding protein in osteoclasts in a similar manner to its behaviour in the intestine. Certainly excess of vitamin D has effects on bone cells similar to those of PTH in that it mobilizes bone calcium and produces hypercalcaemia. In vitamin D deficiency, production of PTH is greatly increased in an attempt to compensate for the chronic hypocalcaemia. 

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