Divalent Cation Mg

8/9/2019 Divalent Cation Mg

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4

Divalent CationMetabolism: Magnesium

Magnesium is an essential intracellular cation. Nearly 99% of thetotal body magnesium is located in bone or the intracellularspace. M agnesium is a critical cation and cofactor in numerous

intracellular processes. It is a cofactor for adenosine triphosphate; animportant membrane stabilizing agent; required fo r the structural integrityof numerous intracellular proteins and nucleic acids; a substrate or cofac-tor for important enzymes such as a denosine triphosphata se, gua nosinetriphosphatase, phospholipase C, adenylate cyclase, and guanylatecyclase; a required cofactor for the activity of over 300 other enzymes; aregulator of ion channels; an important intracellular signaling molecule;and a modulator of oxidative phosphorylation. Finally, magnesium isintimately involved in nerve conduction, muscle contraction, potassiumtransport, and calcium channels. Because turnover of magnesium in boneis so low, the short-term body requirements are met by a balance ofgastrointestinal absorption and renal excretion. Therefore, the kidneyoccupies a central role in magnesium balance. Factors that modulate andaffect renal magnesium excretion can have profound effects on magne-sium balance. In turn, magnesium balance affects numerous intracellularand systemic processes [112].

In the presence of normal renal function, magnesium retention andhypermagnesemia are relatively uncommon. Hypermagnesemia inhibitsmagnesium reabsorption in both the proximal tubule and the loop ofHenle. This inhibition of reabsorption leads to an increase in magnesiumexcretion and prevents the development of dangerous levels of serummagnesium, even in the presence of above-normal intake. However, infamilial hypocalciuric hypercalcemia, there appears to be an abnormali-

ty of the thick ascending limb of the loop of Henle that prevents excre-tion of calcium. This abnormality may also extend to Mg. In familialhypocalciuric hypercalcemia, mild hypermagnesemia does not increasethe renal excretion of magnesium. A similar abnormality may be causedby lithium [1,2,6,10]. The renal excretion of magnesium also is belownormal in states of hypomagnesemia, decreased dietary magnesium,dehydration a nd vo lume depletion, hypocalcemia, hypo thyroidism, andhyperparathyroidism [1,2,6,10].

Ja m es T. M cCa r t hy R a j iv K u m a r

CHA P T E R


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4.2 Disorders of Water, Electrolytes, and Acid-Base

Magnesium Distribution

TOTAL BODY MAGNESIUM (MG) DISTRIBUTION

Location

Bone

Muscle

Soft tissue

Erythrocyte

Serum

Total

Percent of Total

53

27

19.2

0.5

0.3

Mg Content, mmol*

530

270

192

5

3

1000

Mg Content, mg*

12720

6480

4608

120

72

24000

*data typical for a 70 kg adult

FIGURE 4-1

Tota l distribut ion of ma gnesium (M g) inthe body. M g (molecular w eight, 24.305 D)

is predominantly distributed in bone, mus-

cle, a nd soft tissue. Tota l body Mg content

is about 24 g (1 mol) per 70 kg. Mg in

bone is adsorbed to the surface of hydroxy-

apatite crystals, and only about one third is

readily availab le as an exchangeable pool.

Only about 1% of the total body Mg is in

the serum and interstitial fluid

[1,2,8,9,11,12].

Proteins, enzymes,

citrate,

ATP, ADP

Intracellular magnesium (Mg)

Membrane

proteins

Mitochondria

Ca Mg

ATPase

Endoplasmic

reticulum

Mg2+

DNA

RNA

Mg2+

FIGURE 4-2

Intracellular d istribution of ma gnesium (Mg). O nly 1% to 3% of

the tota l intracellular M g exists as the free ionized form of M g,

w hich has a closely regulated concentrat ion of 0.5 to 1.0 mmol.

Tota l cellular Mg concentrat ion can vary from 5 t o 20 mmol,

depending on the type of tissue studied, with the highest Mg con-

centrations being found in skeletal and cardiac muscle cells. Our

understanding o f the concentration a nd distribution of intra cellular

Mg has been facilitated by the development o f electron microprobe

analysis techniques and fluorescent dyes using microfluorescence

spectrometry. Intracellular Mg is predominantly complexed to

organic molecules (eg, adenosine triphosphatase [ATPase], cell and

nuclear membrane-associated proteins, D NA a nd R NA, enzymes,

proteins, and citrates) or sequestered within subcellular organelles

(mitochondria and endoplasmic reticulum). A heterogeneous distri-bution of Mg occurs within cells, with t he highest concentrations

being found in the perinuclear areas, which is the predominant site

of endoplasmic reticulum. The concentration of intracellular free

ionized M g is tightly regulated by intracellular sequestrat ion and

complexation. Very little change occurs in the concentration of

intracellular free Mg, even w ith large varia tions in the concentra-

tions of to tal intra cellular o r extracellular M g [1,3,11]. ADP

adenosine diphosphate; ATPadenosine triphosphate; Ca + ion-

ized calcium.


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4.3Divalent Cation Metabolism: Magnesium

?

Extracellular

Extracellular

Cellular

-Adrenergic receptor

Adenylyl cyclase

Mitochondrion

Nucleus

cAMP

++

ADP ATPMgPi

Ca2+

Ca2+

pK C D.G. +IP3

Muscarinic receptor orvasopressin receptor

Plasma membrane

Plasma membrane

ATP+Mg2+

[Mg2+] =0.7-1.2mmol

[Mg2+] =0.5mmolMg2+

Mg2+

Mg2+

Mg2+

Na+(Ca2+?)

Na+

(Ca2+

?)

Mg2+?

?

+?

+?

+?

?

Mg2+?

E.R. or

S.R.+

Ca2+

Mg2+?

FIGURE 4-3

Regulation of intracellular magnesium (Mg2+ ) in the mammalian cell. Shown is an exam-

ple of Mg2+ movement between intracellular and extracellular spaces and within intracel-

lular compartments. The stimulation of adenylat e cyclase activity (eg, through stimulation

of -adrenergic receptors) increases cyclic adenosine monophosphate (cAMP). The

increase in cAMP induces extrusion of Mg from mitochondria by way of mitochondrial

adenine nucleotide translocase, w hich exchanges 1 M g2+ -adenosine tr iphospha te (ATP)

for adenosine diphosphate (AD P). This slight increase in cyto solic Mg 2+ can then be

extruded through the plasma membrane by way of a Mg-cation exchange mechanism,

which may be activated by either cAMP or Mg. Activation of other cell receptors ( eg,

muscarinic receptor or vasopressin receptor) ma y a lter cAMP levels or produce diacyl-

Intracellular Magnesium Metabolism

glycerol (D AG). DAG a ctivates Mg influx

by way of protein kinase C (pK C) activity.Mitochondria may a ccumulate Mg b y the

exchange of a cytosolic Mg2+ -ATP for a

mitochondria l matr ix Pi mo lecule. This

exchange mechanism is C a2+ -activated and

bidirectional, depending on the concentra-

tions of Mg2+ -ATP and Pi in the cytosol

and mitochondria. Inositol 1,4,5-trisphos-

phate (IP3) may also increase the release of

Mg from endoplasmic reticulum or sar-

coplasmic reticulum (ER or SR, respective-

ly), which a lso has a po sitive effect on this

M g2+ -ATP-Pi exchanger. Other potential

mechanisms affecting cyt osolic Mg include

a hypothetical C a 2+ -Mg 2+ exchanger locat-

ed in the ER and transport proteins that

can allow t he accumulation of M g w ithin

the nucleus or ER. A balance must exist

between passive entry of Mg into the cell

and an a ctive efflux mechanism because

the concentration gradient favors the

movement of extra cellular M g (0.71.2

mmol) into the cell (free Mg, 0.5 mmol).

This Mg extrusion process may be energy-

requiring or may be coupled to the move-

ment of other ca tions. The cellular mo ve-

ment of Mg generally is not involved in the

transepithelial transport of Mg, which is

primarily passive and occurs betw een cells

[13,7]. (FromRomani and coworkers [3];

w ith permission.)


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Mg2+

Mg2+

Mg2+

Mg2+

Mg2+

Mg2+

Mg2+

MgtB MgtA

CorA

ATP

ADP

ATP

ADP

37 kDa?

Cytosol

ExtracellularOuter membrane

Mg2+ Periplasm

A

1 2 3 4

Cytoplasm

Periplasm

Cytoplasm

Periplasm

MgtA and MgtB CorA

5 6 7 8 1

N

N

2 39 10

CC

B

Gastrointestinal

absorption of

dietary magnesium (Mg)

Site

Stomach

DuodenumJejunum

ProximalIleum

DistalIleum

Colon

0

0.63

1.25

1.88

1.25

0.63

0

15

30

45

30

15

0

5

10

15

10

5

mmol/day

Mg absorption %of intake

absorptionmg/day

Total*

*Normal dietary Mg intake=300 mg (12.5 mmol) per day

5.6 135 45

FIGURE 4-4

A, Transport systems of ma gnesium (Mg). Specific membrane-

associated Mg transport proteins only have been described in bac-

teria such as Salmonella. Although similar transport proteins are

believed to b e present in mamma lian cells based on nucleotide

sequence analysis, they have not yet been demonstrated. BothMgtA and MgtB (molecular weight, 91 and 101 kDa, respective-

ly) are members of the adenosine triphosphatase (ATPase) family

of transport proteins. B, Both of these transport proteins have six

C-terminal and four N -terminal membra ne-spanning segments,

with both t he N- and C -terminals within the cytoplasm. Both

proteins transport Mg with its electrochemical gradient, in con-

trast to other known ATPase proteins that usually transport ions

against their chemical gradient. Low levels of extracellular Mg

are capable of increasing transcription of these transport proteins,

which increases transport of Mg into Salmonella. The CorA sys-

tem has three membrane-spanning segments. This system mediates

Mg influx; however, at extremely high extracellular Mg concen-trations, this protein can also mediate Mg efflux. Another cell

membrane Mg transport protein exists in erythrocytes (RBCs).

This RBC N a + -Mg2+ antiporter (not shown here) facilitates the

outward movement of Mg from erythrocytes in the presence of

extracellular Na + and intracellular a denosine triphosphate (ATP)

[4,5]. ADPadenosine diphosphate; Ccarbon; Nnitrogen.

(FromSmith and M aguire [4]).

FIGURE 4-5

Gastrointestinal absorption of dietary intake of magnesium (Mg).

The norma l adult d ietary inta ke of Mg is 300 to 360 mg/d (12.515

mmol/d). A Mg inta ke of a bout 3.6 mg/kg/d is necessary to main ta in

Mg balance. Foods high in Mg content include green leafy vegetables

(rich in M g-conta ining chlorophyll), legumes, nuts, seafo ods, a nd

meats. Ha rd w ater conta ins abo ut 30 mg/L of Mg. D ietary intake is

the only source by which the body can replete Mg stores. Net intesti-

nal M g absorption is affected by t he fractional Mg a bsorption w ithin

a specific segment of intestine, the length of that intestinal segment,

and transit time of the food bolus. Approximately 40% to 50% of

dietary Mg is absorbed. Both the duodenum and jejunum have a

high fract ional a bsorption o f M g. These segments of intestine are rel-

atively short, how ever, a nd the t ransit time is rapid. Therefore, their

relative contribution to total Mg absorption is less than that of the

ileum. In the intact animal, most of the Mg absorption occurs in theileum and colon. 1,25-dihydrox y-vitamin D 3 may mildly increase the

intestinal absorption of Mg; however, this effect may be an indirect

result of increased calcium absorption induced by t he vitamin.

Secretions of the upper intestinal tract contain approximately 1

mEq/L of M g, w hereas secretions from the low er intestinal tr act con-

tain 15 mEq/L of M g. In states of nausea, vomiting, or na sogastric

suction, mild to moderate losses of Mg occur. In diarrheal states, Mg

depletion can occur rapidly owing to both high intestinal secretion

and lack of Mg absorption [2,6,813].

Gastrointestinal Absorption of Magnesium


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0 3 6 9 12 15 18 21 24

[Mg] in bicarbonate saline,m Eq/ L

0

1

2

3

4

5

6

7

8

9

3 13

3

6

12

22

3

Mgtransported,

Eq/h

10

A

0 10 20 30 40

Oral magnesium dose m,m m ol

0

1

2

3

4

5

6

PhysiologicalMg-intake,m m ol/ d

7

Magnesiumabsorbed

MMg,mm

ol

B

0 20 40 60 80

Mg intake,m Eq/ m eal

0

2

4

6

8

10

NetMgabsorption,m

Eq/10hrs

C

Mechanism ofintestinal magnesium absorption

Mg2+

Nucleus

Mg2+

K+Na+

ATPase

LumenMg2+

Mg2+

A

B

FIGURE 4-6

Intestinal magnesium (Mg) absorption. In rats, the intestinal Mg

absorption is related to the luminal Mg concentration in a curvilin-ear fashion (A). This same phenomenon has been observed in

humans (B and C). The hyperbolic curve (dotted li nein B and C)

seen at low doses and concentrations may reflect a saturable tran-

scellular process; w hereas t he linear function (dashed li nein B and

C) at higher Mg intake may be a concentration-dependent passive

intercellular Mg absorption. Alternatively, a n intercellular pro cess

that can vary its permeability to Mg, depending on the luminal Mg

concentration, could explain these findings (seeFig. 4-7) [1315]. (A,

FromKayne and Lee [13]; B, fromRoth and Wermer [14]; C, from

Fine and cow orkers [15]; wit h permission.)

FIGURE 4-7

Proposed pat hw ays fo r movement of magnesium (M g) across the intestinal epithelium. Tw o

possible routes exist for the absorption of Mg across intestinal epithelial cells: the transcel-

lular route and the intercellular pathway. Although a transcellular route has not yet been

demonstrated, its existence is inferred from several observations. No large chemical gradient

exists for Mg movement across the cell membrane; however, a significant uphill electrical

gradient exists for the exit of Mg from cells. This finding suggests the existence and partici-

pation of an energy-dependent mechanism for extrusion of Mg from intestinal cells. If such

a system exists, it is believed it would consist of two stages. 1) Mg would enter the apical

membrane of intestinal cells by way of a passive carrier or facilitated diffusion. 2) An active

Mg pump in the basolateral section of the cell would extrude Mg. The intercellular move-

ment of Mg has been demonstrated to occur by both gradient-driven and solvent-drag

mechanisms. This intercellular path may be the only means by which Mg moves across the

intestinal epithelium. The change in transport rates at low Mg concentrations would reflect

changes in the openness of this pathw ay. High concentrations of luminal Mg (eg, after a

meal) are capable of altering the morphology of the tight junction complex. High local Mg

concentrations near the intercellular junction also can affect the activities of local mem-

brane-associated proteins (eg, sod ium-pota ssium a denosine triphosphate [Na-K ATPase])

near the tight junction and affect its permeability (seeFig. 4-6) [1315].


6/12


Afferentarteriole

Ionized MgProtein-bound MgComplexed Mg

*Normal total serum Mg =1.72.1 mg/dL (0.700.9 mmol/L)

60%33%7%

Glomerularcapillary

Mg2+-protein

Mg2+-ultrafilterable

Bowman'sspace

Proximaltubule

Efferentarteriole

Mg2+ionized Mg2+complexed

Mg2+ %of totalserum Mg2+

Juxtamedullarynephron

Superficial corticalnephron

Filtered

Mg2+(100%)

05%

Excreted(5%)

510%

65%65%

Filtered

Mg2+

(100%)

20%

20%

FIGURE 4-8

The glomerular filtra tion o f mag nesium (Mg). Tota l serum Mgconsists of ionized, complexed, a nd prot ein bound fra ctions, 60%,

7%, and 33% of total, respectively. The complexed Mg is bound

to molecules such as citrate, oxalate, and phosphate. The ultrafil-

terable Mg is the total of the ionized a nd complexed fra ctions.

Norma l tota l serum Mg is approximately 1.7 to 2.1 mg/dL (about

0.700.90 mmol/L) [1,2,79,11, 12].

Renal Handling of Magnesium

FIGURE 4-9

The renal hand ling of magnesium (Mg 2+ ). Mg is filtered at the

glomerulus, with the ultrafilterable fraction of plasma Mg entering

the proximal convoluted tubule (PCT). At the end of t he PCT, the

Mg concentration is approximately 1.7 times the initial concentra-

tion of Mg and about 20% of the filtered Mg has been reab-

sorbed. M g reabsorption o ccurs passively through pa racellular

pathwa ys. Hyd rated M g has a very large radius that d ecreases its

intercellular permeability in the PC T w hen compared w ith sodi-

um. The smaller hyd rated rad ius of sodium is 50% to 60% reab-

sorbed in t he PCT. N o clear evidence exists of transcellular reab-

sorption or secretion of M g w ithin the mammalian PC T. In thepars recta of the proximal stra ight tubule (PST), Mg reab sorption

can continue to occur by way of passive forces in the concentrat-

ing kidney. In states of normal hydration, however, very little Mg

reab sorptio n occurs in the PST. Within the thin descending limb of

the loop of Henle, juxtamedullary nephrons are capable of a small

amount of Mg reabsorption in a state of antidiuresis or Mg deple-

tion. This reab sorption do es not occur in superficial cortica l

nephrons. No data exist regarding Mg reabsorption in the thin

ascending limb of the loop of Henle. No Mg reabsorption occurs

in the medullary portion of the thick ascending limb of the loop of

H enle; w hereas nearly 65% of the filtered load is absorbed in the

cortical thick ascending limb of the loop of Henle in both jux-

tamedullary and superficial cortical nephrons. A small amount of

Mg is absorbed in the distal convoluted tubule. Mg transport in

the connecting tubule has not been well qua ntified. Little reab-sorption occurs and no evidence exists of M g secretion w ithin the

collecting duct. N ormally, 95% of the filtered M g is reabsorbed

by the nephron. In states of Mg depletion the fractional excretion

of Mg can decrease to less than 1%; whereas Mg excretion can

increase in states of a bove-normal M g intake, provided no evi-

dence of renal failure exists [1,2,69,11,12].


7/12


Mg absorption in cTAL

2Na+

Mg

Mg

Mg Mg 0.5mmol

~1.0mmol

~1.0mmol

+8mV 0mV78mV

3Na+ 3Na+

6Cl

2Cl

1Cl

2K+

3K+

2K+

4Cl

3K+

6

4

5

1

2

3

A

FIGURE 4-10

M agnesium (Mg) reabsorpt ion in the cortica l thick ascending limb (cTAL) of t he loop of

Henle. Most Mg reabsorption w ithin the nephron occurs in the cTAL ow ing primarily to

voltage-dependent Mg flux through the intercellular tight junction. Transcellular Mg

movement occurs only in response to cellular metabolic needs. The sequence of events nec-

essary to generate the lumen-positive electrochemical gradient that drives Mg reabsorption

is as follows: 1) A basolateral sodium-potassium-adenosine triphosphatase (Na + -K+ -ATPase) decreases intracellular sodium, generating an inside-negative electrical potential

difference; 2) Intracellular K is extruded by an electroneutral K-Cl (chloride) cotrans-

porter; 3) Cl is extruded by way of conductive pathways in the basolateral membrane; 4)

The apical-luminal Na-2Cl-K (furosemide-sensitive) cotransport mechanism is driven by

the inside-negative potential difference and decrease in intracellular Na; 5) Potassium is

recycled back into the lumen by w ay o f an apical K conductive channel; 6) Passage of

approximately 2 N a molecules for every C l molecule is allowed by the paracellular pa th-

w ay (intercellular tight junction), w hich is cat ion permselective; 7) Mg reabsor ption occurs

passively, by way of intercellular channels, as it moves down its electrical gradient

[1,2,6,7]. (Adapted fromde Rouffignac a nd Q uamme [1].)

18 15129 6 3

Vt,m V

JMg

,p m o l.m in 1.m m 1

0.8

0.6

0.4

0.2

0.2

0.4

(8)

(7)

(15)

0.6

0.8

3 6 9 12 15 18

FIGURE 4-11

Volta ge-dependent net magnesium (Mg) flux in t he cortical t hick

ascending limb (cTAL). Within the isolated mouse cTAL, Mg flux

(JM g) occurs in response to volta ge-dependent mechanisms. With

a relative lumen-positive tra nsepithelial pot ential d ifference (Vt),

Mg reabsorption increases (positive JM g). Mg reabsorption equals

zero when no voltage-dependent difference exists, and Mg is

capable of moving into the tubular lumen (negative J M g) when alumen-negative voltage difference exists [1,16]. (Fromdi Stefano

and coworkers [16]).


8/12


*

0

0.2

0.4

C

*

C

0.6

0.8

1.0

JMg2+AVP

C C

GLU

Netfluxes,pm

ol

m

in

1

m

m

1

*

*

C C

PTH

C C

HCT

C

*

C

ISO

C

*

C

INS

FIGURE 4-12

Effect of ho rmones on magnesium (Mg)

transport in the cortical thick ascending

limb (cTAL). In the presence of a rginine

vasopressin (AVP), glucagon (GL U), human

calcitonin (HCT), parathyroid hormone

(PTH), 1,4,5-isoproteronol (ISO), andinsulin (INS), increases occur in Mg reab-

sorption from isolated segments of mouse

cTALs. These hormones have no effect on

medullary TAL segments. As already has

been shown in Figure 4-3, these hormones

af fect intracellular second messengers

and cellular Mg movement. These hor-

mone-induced a lterations can affect t he

paracellular permeability of the intercellular

tight junction. These changes may also

affect t he transepithelial volta ge across the

cTAL. Both o f these forces fa vor net M g

reabso rption in the cTAL [1,2,7,8].

Asterisksignificant change from preceding

period; JM gMg flux; Ccontrol, absenceof hormone. (Adapted fromde Rouffignac

and Qua mme [1].)

CAUSES OF MAGNESIUM (Mg) DEPLETION

Poor Mg intake

StarvationAnorexia

Protein calorie malnutrition

No Mg in intravenous fluids

Renal losses

se e Fig. 4-14

Increased gastrointestinal Mg losses

Nasogastric suction

Vomiting

Intestinal bypass for obesity

Short-bowel syndrome

Inflammatory bowel disease

Pancreatitis

Diarrhea

Laxative abuse

Villous adenoma

Other

LactationExtensive burns

Exchange transfusions

FIGURE 4-13

The causes of magnesium (Mg) depletion. Depletion of Mg can

develop as a result of low intake or increased losses by w ay of the

gastrointestinal tract, the kidneys, or other routes [1,2,813].

Magnesium Depletion


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10/12


Altered synthesisof eicosanoids

Insulinresistance

Plateletaggregation

Enhanced AIIaction

Hypertension

Aldosterone

Increased vasomotor tone Na+reabsorption

(PGI2, :TXA

2, and 12-HETE)

Magnesium deficiency

Normal(1.72.1 mg/dL)

Normal(>24 mg/24 hrs)

NormalMg retention

Normal

Mgretention

No Mgdeficiency

Check fornonrenal causes

Mg deficiencypresent

Renal Mg wasting

Tolerance Mg test(se eFigure 418)

Low(


11/12


MAGNESIUM SALTS USED IN MAGNESIUM REPLACEMENT THERAPY

Magnesium salt

Gluconate

Chloride

Lactate

Citrate

Hydroxide

Oxide

Sulfate

Milk of Magnesia

Chemical formula

Cl2H22MgO14

MgCl2. (H2O)6

C6H10MgO6

C12H10Mg3O14

Mg(OH)2

MgO

MgSO4. (H2O)7

Mg content, mg/g

58

120

120

53

410

600

100

Examples*

Magonate

Mag-L-100

MagTab SR*

Multiple

Maalox, Mylanta, Gelusil

Riopan

Mag-Ox 400

Uro-Mag

Beelith

IV

IV

Oral epsom salt

PhillipsMilk of Magnesia

Mg content

27-mg tablet54 mg/5 mL

100-mg capsule

84-mg caplet

4756 mg/5 mL

83 mg/ 5 mL and 63-mg tablet

96 mg/5 mL

241-mg tablet

84.5-mg tablet

362-mg tablet

10%9.9 mg/mL

50%49.3 mg/mL

97 mg/g

168 mg/ 5 mL

Diarrhea

+

+

++

++

++

++

++

++

Da ta fr om McLean [9], Al-Ghamdi and coworkers [11], Oster and Epstein [19], and PhysiciansDesk Reference [20].

*Magonate, Fleming & Co, Fenton, MD; MagTab Sr, Niche Pharmaceuticals, Roanoke, TX; Maalox, Rhone-Poulenc Rorer Pharmaceutical, Collegeville, PA; Mylanta,J & J-Merck Consumer Pharm, Ft Washinton, PA; Riopan, Whitehall Robbins Laboratories, Madison, NJ; Mag-Ox 400and Uro-Mag, Blaine, Erlanger, KY; Beelith,Beach Pharmaceuticals, Conestee, SC; PhillipsMilk of Magnesia, Bayer Corp, Parsippany, NJ.

FIGURE 4-19

Ma gnesium (Mg) salts tha t ma y b e used in M g replacement therapy.

GUIDELINES FOR MAGNESIUM (Mg) REPLACEMENT

I.24 g MgSO4IV or IM stat

(24 vials [2 mL each] of 50%MgSO4)

Provides 200400 mg of Mg (8.316.7 mmol Mg)

Closely monitor:

Deep tendon reflexes

Heart rate

Blood pressure

Respiratory rate

Serum Mg (


12/12


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14. Roth P, Werner E: Intestinal absorption of magnesium in man. Int J

Appl Radiat Isotopes1979, 30:523526.

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of ma gnesium from food and supplements. J Clin I nvest1991,

88:396402.

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C a + and Mg+ transport in the cortical thick ascending limb of Henles

loop of the mouse is a voltage-dependent process. Renal Physiol

Biochem1993, 16:157166.

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References

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