Parathyroid hormone release

Brown, EM, Fuleihan, Ge-H, Chen, CJ and Kifor, O, 1990, A comparison of the effects of divalent and trivalent cations on parathyroid hormone release, 3, 5 -cyclic-adenosine monophosphate accumulation, and the levels of inositol phosphates in bovine parathyroid cells, Endocrinology 127 1064-1071... 

Hormone synthesis and release can be initiated by both extrinsic and intrinsic factors.2 Extrinsic factors include various environmental stimuli such as pain, temperature, light, and smell. Intrinsic stimuli include various humoral and neural factors. For instance, release of a hormone can be initiated by other hormones. These occurrences are particularly typical of the anterior pituitary hormones, which are controlled by releasing hormones from the hypothalamus. Hormonal release can be influenced by neural input a primary example is the sympathetic neural control of epinephrine and norepinephrine release from the adrenal medulla. Other intrinsic factors that affect hormone release are the levels of ions and metabolites within the body. For instance, parathyroid hormone release is governed directly by the calcium concentration in the bloodstream, and the release of... 

Parathyroid hormone (PTH) plays a crucial role in regulating concentrations of calcium and phosphorus in the extracellular fluid. The major signal for parathyroid hormone release is low extracellular levels of free calcium ion. PTH acts on 3 major targets—small intestine, kidney, and bone— to restore calcium ion concentrations in the extracellular fluid to the normal range if they fall too low. 

B30. Brown, E. M., Wilson, R. E., Eastman, R. C., et al., Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure. J. Clin. Endocrinol. Metab. 54, 172-179 (1982). 

Lithium is one of the group lA alkali metals (like potassium and sodium) and is not normally present in the body. It acts predominantly through the phosphatidylinositol (PI) second messenger system, causing alterations in calcium- and protein kinase C (PKC)-mediated processes. Lithium can also alter the adenylate cyclase (AC) system, but this action is probably related to its toxic effects. Many calcium-dependent systems may be affected by lithium, among them regulation of receptor sensitivity, parathyroid hormone release, and proper functioning of intracellular microtubule structures. - ... 

The metabolically active form of vitamin D. Vitamin D is initially hydroxylated by the liver to 25-hydroxychoIecaIciferol and a further hydroxylation takes place in the kidney to form the dihydroxy compound. 1,25-dihydroxycholecalciferol increases calcium absorption from the intestine and, in conjunction with parathyroid hormone, releases calcium from bone. 

Fitzpatrick, L. A. (1990). "Differences in the actions of calcium versus lanthanum to influence parathyroid hormone release." Endocrinology, 127(2), 711-5. 

Brown, E. M., Gardner, D. G., Windeck, R. A., and Aurbach, G. D., 1979, Cholera toxin stimulates 3, 5 -adenosine monophosphate accumulation and parathyroid hormone release from dispersed bovine parathyroid glands. Endocrinology 104 218. 

Factors controlling calcium homeostasis are calcitonin, parathyroid hormone(PTH), and a vitamin D metabolite. Calcitonin, a polypeptide of 32 amino acid residues, mol wt - SGOO, is synthesized by the thyroid gland. Release is stimulated by small increases in blood Ca " concentration. The sites of action of calcitonin are the bones and kidneys. Calcitonin increases bone calcification, thereby inhibiting resorption. In the kidney, it inhibits Ca " reabsorption and increases Ca " excretion in urine. Calcitonin operates via a cyclic adenosine monophosphate (cAMP) mechanism. 

Parathyroid hormone, a polypeptide of 83 amino acid residues, mol wt 9500, is produced by the parathyroid glands. Release of PTH is activated by a decrease of blood Ca " to below normal levels. PTH increases blood Ca " concentration by increasing resorption of bone, renal reabsorption of calcium, and absorption of calcium from the intestine. A cAMP mechanism is also involved in the action of PTH. Parathyroid hormone induces formation of 1-hydroxylase in the kidney, requited in formation of the active metabolite of vitamin D (see Vitamins, vitamin d). 

Molecules released by exocytosis fall into three categories (1) They can attach to the cell surface and become peripheral proteins, eg, antigens. (2) They can become part of the extracellular matrix, eg, collagen and glycosaminoglycans. (3) They can enter extracellular fluid and signal other cells. Insulin, parathyroid hormone, and the catecholamines are all packaged in gran-... 

Discuss functions and factors regulating release of the following hormones thyroid hormones, calcitonin, parathyroid hormone, catecholamines, aldosterone, cortisol, adrenal androgens, insulin, and glucagon... 

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. 

The a ns wer is a. (Hardman, pp 1525-1528.) Pa r a thyroid ho r m o ne is synthesized by and released from the parathyroid gland increased synthesis of PTI1 is a response to low serum Ca concentrations. Resorption and mobilization of Ca and phosphate from bone are increased in response to elevated PTI1 concentrations. Replacement of body stores of Ca is enhanced by the capacity of PTH to promote increased absorption of Ca by the small intestine in concert with vitamin D, which is the primary factor that enhances intestinal Ca absorption. Parathyroid hormone also causes an increased renal tubular reabsorption of Ca and excretion of phosphate. As a consequence of these effects, the extracellular Ca concentration becomes elevated. 

Hypocalcemia (below-normal blood calcium) stimulates release of parathyroid hormone (PTH), which in turn binds to receptors on cells of the renal proximal tubules. The receptors are coupled through cAMP to activation of a la-hydroxylase important for the final, rate-hmiting step in the conversion of vitamin D to 1,25-DHCC (dihydroxycholecalciferol or caldtriol). 

Keywords FoUide-stimulating hormone gain of function gonadotropin-releasing hormone (GnRHR) G protein-coupled receptor loss of function luteinizing hormone melanocortin monogenic disease parathyroid hormone rhodopsin thyrotropin. 

There are four parathyroid glands, which are situated behind the thyroid. They produce parathyroid hormone (PTH), a peptide which interacts with vitamin D to control the level of calcium in the blood. PTH stimulates release of calcium from bone and increases the uptake of calcium by the kidney tubules from the glomerular hltrate. 

The Ca -selective hormones calcitriol, parathyroid hormone, and calcitonin influence this interaction in the bone cells. Parathyroid hormone promotes Ca "" release by promoting the release of cytokines by osteoblasts. In turn, the cytokines stimulate the development of mature osteoclasts from precursor cells (bottom). Calcitonin inhibits this process. At the same time, it promotes the development of osteoblasts (top). Osteoporosis, which mainly occurs in women following the menopause, is based (at least in part) on a reduc-... 

Calcitriol and parathyroid hormone, on the one hand, and calcitonin on the other, ensure a more or less constant level of Ca "" in the blood plasma and in the extracellular space (80-110 mg 2.0-2.6 mM). The peptide parathyroid hormone (PTH 84 AA) and the steroid calcitriol (see p. 374) promote direct or indirect processes that raise the Ca "" level in blood. Calcitriol increases Ca "" resorption in the intestines and kidneys by inducing transporters. Parathyroid hormone supports these processes by stimulating calcitriol biosynthesis in the kidneys (see p. 330). In addition, it directly promotes resorption of Ca "" in the kidneys (see p. 328) and Ca "" release from bone (see B). The PTH antagonist calcitonin (32 AA) counteracts these processes. 

Osteoclast. A large multinuclear cell associated with the absorption and removal of bone, osteoclasts become highly active in the presence of parathyroid hormone, causing increased bone resorption and release of bone salts (phosphoms, and especially calcium) into the extracellular fluid. Ovalbumin. An albumin obtainable from the whites of eggs. 

Regulation of 25-hydroxycholecalciferol 1-hydroxylase 1,25-diOH D3 is the most potent vitamin D metabolite. Its formation is tightly i regulated by the level of plasma phosphate and calcium ions (Figure 28.24). 25-Hydroxycholecalciferol1 -hydroxylase activity is I increased directly by low plasma phosphate or indirectly by bw I plasma calcium, which triggers the release of parathyroid hormone I... 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

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