Calcium-induced secretion

Horse platelets contain a large nonmetabohe pool of serotonin and adenine nucleotides within dense bodies (White et al. 1976). Calcium ionophore (A23187) and high doses of thrmnbin (0.4 unitsAnl), but not collagen, ADP, or arachadonic acid, induced secretion of ATP and/or C-serotonin (Weiss et al. 1990, Boudreaux et al. 1988). 

Both cAMP and intracellular calcium are used as second messengers by this cell. The former mediates adrenergic and histamine-induced secretion, the latter CCK and cholinergic (Ms) stimulation. 

PTH is a single-chain polypeptide that is released from the parathyroid when there is a decrease in the calcium concentration in extracellular fluid. The calcium-sensing receptor (acting as the thermostat for calcium) is found on the parathyroid gland, where it detects small perturbations in serum ionized calcium. The decline in serum calcium induces an increase in PTH secretion. PTH has the effect of restoring extracellular calcium concentrations by stimulating the resorption of bone to release... 

Jefferson KK, Smith MF Jr, Bobak DA Roles of intracellular calcium and NF-kappa B in the Clostridium difficile toxin A-induced up-regulation and secretion of IL-8 from human monocytes. JImmunol 1999 163 5183-5191. 

The importance of insulin as a mediator of the hypercalciuric effect of arginine infusion was also evident from studies conducted in chronically diabetic rats, where diabetes was induced by strepto-zotocin (23). Animals were injected with streptozotocin prior to arginine infusion 100 mg/kg i.p. was given on the seventh day before, followed by 25 mg/kg six days before the arginine infusion and renal clearance studies. In contrast to non-diabetic controls, diabetic animals did not increase their urinary calcium excreted (per ml glomerular filtrate) in response to the arginine infusion, nor did the arginine stimulate insulin secretion. 

The suppression of PTH secretion from the parathyroid gland that accompanies the constitutive activation of the CASR makes the disorder difficult to recognize and treat. In some cases, it has been reported that seizures can be intractable. The abnormal set point of calcium regulation complicates treatment with calcitriol and dietary calcium supplementation because the CASR expressed in the kidney controls calcium excretion. The constitutively activated CASR mutant induces hypercalciuria, which may compound the hypocalcemia (42). 

Orotic acid in the diet (usually at a concentration of 1 per cent) can induce a deficiency of adenine and pyridine nucleotides in rat liver (but not in mouse or chick liver). The consequence is to inhibit secretion of lipoprotein into the blood, followed by the depression of plasma lipids, then in the accumulation of triglycerides and cholesterol in the liver (fatty liver) [141 — 161], This effect is not prevented by folic acid, vitamin B12, choline, methionine or inositol [141, 144], but can be prevented or rapidly reversed by the addition of a small amount of adenine to the diets [146, 147, 149, 152, 162]. The action of orotic acid can also be inhibited by calcium lactate in combination with lactose [163]. It was originally believed that the adenine deficiency produced by orotic acid was caused by an inhibition of the reaction of PRPP with glutamine in the de novo purine synthesis, since large amounts of PRPP are utilized for the conversion of orotic acid to uridine-5 -phosphate. However, incorporation studies of glycine-1- C in livers of orotic acid-fed rats revealed that the inhibition is caused rather by a depletion of the PRPP available for reaction with glutamine than by an effect on the condensation itself [160]. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

Plasma calcium concentration is the principal factor regulating PTH synthesis and release. The increase in PTH synthesis and secretion induced by hypocalcemia is believed to be mediated through activation of parathyroid gland adenylyl cyclase and a subsequent increase in intracellular cyclic adenosine monophosphate (cAMP). 

Kimura, M., I. Kimura, and F. J. Chen. Combined potentiating effects of by-akko-ka-ninjin-to, its constituents, rhizomes of anemarrhena, asphodeloides, timosaponin a-III, and calcium on pilocarpine-induced saliva secretion in strep-tozocin-diabetic mice. Biol Pharm Bull 1996 19(7) 926-931. 

Mechanism of Action An antihyperglycemic that stimulates release of insulin from beta cells of the pancreas by depolarizing beta cells, leading to an opening of calcium channels. Resulting calcium influx induces insulin secretion. Therapeutic Effect Lowers blood glucose concentration. 

Calcium ions entering cells from the outside or released from internal stores trigger many biological responses (see Box 6-D). Within cells Ca2+ often accumulates in mitochondria, in the ER, or in vesicles called calciosomes.265 Release of the stored Ca2+ is induced by hormones or by nerve impulses. For example, impulses flow from the nerve endings into the muscle fibers and along the invaginations of the plasma membrane called transverse tubules (Chapter 19). There they induce release of Ca2+ from the ER. The released ions activate enzymes266 and induce contraction of the muscle fibers. In many cells, Ca2+ causes release of secreted materials, for example, neurotransmitters in the brain 267/268... 

Reshkin SJ, Guerra L, Bagorda A, Debellis L, Cardone R, Li AH, Jacobson KA, Casavola V (2000) Activation of A adenosine receptor induces calcium entry and chloride secretion in A6 cells. J Membr Biol 178(2) 103-113... 

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