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[Ca++]

Vitamin D3 activation PTH

Intestinal Ca++ reabsorptionRenal Ca++ reabsorptionCa++ release from bones

Figure 2910

372 Unit V The Body Fluids and Kidneys

Compensatory responses to decreased plasma ionized calciumconcentration mediated by parathyroid hormone (PTH) andvitamin D.

calcium concentration falls below normal, the

parathy- roid glands are directly stimulated by thelow calciumlevels to promote increased secretion ofPTH. This hormone then acts directly on the bonesto increase the resorption of bone salts (release ofsalts from the bones) and, therefore, to release largeamounts of calcium into the extracellular fluid,thereby returning calcium levels bac towardnormal. !hen calcium ion concentration is elevated,PTH secretion decreases, so that almost no boneresorption now occurs" instead, excess calcium isdeposited in the bones because of new boneformation. Thus, the day-to-day regulation ofcalcium ion concentration is mediated in large part

by the effect of PTH on bone resorption.

The bones, however, do not have an inexhaustiblesupply of calcium. Therefore, over the long term, theintae of calcium must be balanced with calciumexcretion by the gastrointestinal tract and theidneys. The most important regulator of calciumreabsorption at both of these sites is PTH. Thus,PTH regulates plasma calcium concentrationthrough three maineffects: (! "y stimulating "oneresorption# (2! "y stim$ ulating acti%ation of %itamin&, 'hich then increases intestinal rea"sorption ofcalcium# and (3! "y directly increasing renal tu"ularcalcium rea"sorption (#igure $%&'). The control ofgastrointestinal calcium reab- sorption and calcium

exchange in the bones is dis- cussed elsewhere, andthe remainder of this section focuses on themechanisms that control renal calciumexcretion.

Control of Calcium Excretion

by the Kidneys

ecause calcium is both filtered and reabsorbed inthe idneys but not secreted, the rate of renalcalcium excretion is calculated as

*enal calcium excretion = +alcium filtered- +alcium reabsorbed

nly about per cent of the plasma calcium isionied, with the remainder being bound to the

plasma

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proteins or complexed with anions such asphosphate. Therefore, only about per cent of theplasma calcium can be filtered at the glomerulus./ormally, about %% per cent of the filtered calciumis reabsorbed by the tubules, with only about ' percent of the fil- tered calcium being excreted. 0bout1 per cent of the filtered calcium is reabsorbed inthe proximal tubule, $ to 2 per cent is reabsorbedin the loop of Henle, and 3 to % per cent isreabsorbed in the distal and col- lecting tubules.

This pattern of reabsorption is similar to that forsodium.0s is true with the other ions, calcium excretion

is ad4usted to meet the body5s needs. !ith anincrease in calcium intae, there is also increasedrenal calcium excretion, although much of theincrease of calcium intae is eliminated in thefeces. !ith calcium deple- tion, calcium excretion

by the idneys decreases as a result of enhancedtubular reabsorption.

ne of the primary controllers of renal tubularcalcium reabsorption is PTH. !ith increased levelsof PTH, there is increased calcium reabsorption inthe thic ascending loops of Henle and distal

tubules, which reduces urinary excretion ofcalcium. +on- versely, reduction of PTH promotescalcium excretion by decreasing reabsorption in theloops of Henle and distal tubules.

6n the proximal tubule, calcium reabsorptionusuallyparallels sodium and water reabsorption.Therefore, in instances of extracellular volumeexpansion or increased arterial pressure7both ofwhich decrease proximal sodium and water

reabsorption7there is also reduction in calciumreabsorption and, con- se8uently, increased urinaryexcretion of calcium. +onversely, with extracellularvolume contraction or decreased blood pressure,calcium excretion decreases primarily because ofincreased proximal tubular reabsorption.

0nother factor that influences calciumreabsorption is the plasma concentration of

phosphate. 0n increase in plasma phosphatestimulates PTH, which increases calcium

reabsorption by the renal tubules, thereby reducingcalcium excretion. The opposite occurs withreduction in plasma phosphate concentration.

+alcium reabsorption is also stimulated by meta-bolic acidosis and inhibited by metabolic alalosis.9ost of the effect of hydrogen ion concentration oncalcium excretion results from changes in calciumreabsorption in the distal tubule.

0 summary of the factors that are nown to influ-ence calcium excretion by the renal tubules is shownin Table $%&$.

Regulation of Renal Phosphate

Excretion

Phosphate excretion by the idneys is controlledprimarily by an overflow mechanism that can beexplained as follows: The renal tubules have anormal transport maximum for reabsorbing

phosphate of about .' m9;min. !hen less thanthis amount of phosphate is present in theglomerular filtrate,