Renal calcium reabsorption, mechanism

This paper summarizes our evidence that the mechanism involves protein stimulation of insulin secretion, followed rapidly by insulin inhibition of renal calcium reabsorption. In humans, urinary calcium was proportional to peak postprandial insulin levels in several experiments, after either protein or sucrose was fed. 

The Mechanism of Insulin Inhibition of Renal Calcium Reabsorption... 

The mechanism by which insulin impairs renal calcium reabsorption is still under investigation, but some progress has been made toward revealing that the insulin effect is directly on the renal tissues, rather than an indirect effect on other hormones or metabolites. 

Bone is the body s calcium reservoir. PTH stimulates bone resorption leading to the dissolution of hydroxyapatite and release of calcium and phosphate into the blood. This action of PTH appears to be the major mechanism for the rapid elevation of blood calcium levels. PTH also maintains blood calcium levels by promoting calcium reabsorption from the renal tubules. 

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). 

Renal magnesium wasting is the main mechanism responsible for the hypomagnesemia associated with cisplatin (172), and it can be associated with enhanced tubular reabsorption of calcium and consequent hypocalciuria (173). This dissociation in the renal handling of calcium and magnesium is similar to what is found in Bartter s syndrome. The site of the renal tubular defect in these conditions is not known, but there is evidence that active renal tubular transport systems are disrupted. 

Calcitonin acts on receptors in bone osteoclasts with a resulting reduction of bone resorption, and it also acts on the renal tubular reabsorption of phosphate. The phosphaturic effects are accompanied by diuresis and increased excretion of other electrolytes. Calcitonin and parathyroid hormone act as a dual negative feedback mechanism in controlling calcium in intra- and extracellular fluids. The range of calcitonin assays suitable for laboratory animals is limited, but the hormone can be measured by two-site radioimmunometric assays (Moukhtar et al. 2005). 

The role of 1,25-(OH)20 in the kidney is even less well understood, although its localization in the distal renal tubule cells, specifically in the nuclei, is known. No clear role for l,25-(OH)2D2 in renal tubular reabsorption of phosphorus has been established, and this area remains controversial. There is evidence that 1,25-(OH),D, stimulates renal reabsorption of calcium in the distal tubule but little else is known concerning that mechanism. ... 

General metabolic significance. Vitamin D stimulates intestinal absorption of calcium and phosphate, renal reabsorption of these ions, deposition and mobilization of minerals in the hard tissue, controlling normal calcium and phosphate blood level by means of these processes. Molecular mechanism of the vitamin D effects most frequently conform to the effect of steroid hormones (induction of protein biosynthesis). 

Calcium ion activity in blood is strictly regulated by a hormonal feedback mechanism. When the activity tends to decrease, the parathyroids secrete parathyroid hormone (PTH), which stimulates renal tubular reabsorption of Ca , K , and Na and decreases the reabsorption of phosphate. The net effect is a decreased excretion of Ca , Na" ", and K and an increased excretion of phosphate. PTH stimulates the hydroxylase activity in the kidney, and there is a negative feedback system which means that an increased amount of 1,25(OH)2D3 inhibits this hydroxylation procedure. Other hormones such as prolactin, estrogen, and growth hormone also stimulate hydroxylase activity, as does as a low serum phosphate concentration [6]. 

Mechanisms of Renal Water Reabsorption - Much experimental evidence supports the hypothesis, first advanced by Orloff and Handler, that sodium transport and osmotic water flow that characterizes the physiological response to vasopressin.In a recent study. Chase and Aurbach have Identified two distinct adenyl cyclase systems located In renal membrane fractions of rats, one In the cortex and the other In the medulla.While the medullary enzyme was stimulated by vasopressin, cortex adenyl cyclase was more responsive to parathyroid hormone than vasopressin. The localization of parathyroid-sensitive adenyl cyclcise In renal cortex and vasopressin-sensitive adenyl cyclase in renal medulla appears to be consistent with reports that cellular transfer of calcium and phosphate occurs primarily in the proximal portions of the nephron, and sodium transport and water permeability are stimulated by vasopressin mainly In the collecting tubules. Vasopressin-Induced stimulation of adenyl cyclase In the cortex may reflect Its additional action on the distal tubule. 

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