divalent cation mg
TRANSCRIPT
-
8/9/2019 Divalent Cation Mg
1/12
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
-
8/9/2019 Divalent Cation Mg
2/12
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.
-
8/9/2019 Divalent Cation Mg
3/12
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.)
-
8/9/2019 Divalent Cation Mg
4/12
4.4 Disorders of Water, Electrolytes, and Acid-Base
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
-
8/9/2019 Divalent Cation Mg
5/12
4.5Divalent Cation Metabolism: Magnesium
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].
-
8/9/2019 Divalent Cation Mg
6/12
4.6 Disorders of Water, Electrolytes, and Acid-Base
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].
-
8/9/2019 Divalent Cation Mg
7/12
4.7Divalent Cation Metabolism: Magnesium
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]).
-
8/9/2019 Divalent Cation Mg
8/12
4.8 Disorders of Water, Electrolytes, and Acid-Base
*
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
-
8/9/2019 Divalent Cation Mg
9/12
-
8/9/2019 Divalent Cation Mg
10/12
4.10 Disorders of Water, Electrolytes, and Acid-Base
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(
-
8/9/2019 Divalent Cation Mg
11/12
4.11Divalent Cation Metabolism: Magnesium
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 (
-
8/9/2019 Divalent Cation Mg
12/12
4.12 Disorders of Water, Electrolytes, and Acid-Base
1. de Rouffignac C, Quamme G: Renal magnesium handling and itshormonal control. Physiol Rev1994, 74:305322.
2. Quamme GA: M agnesium homeostasis and renal magnesium han-dling. M iner Electrol yte Metab1993, 19:218225.
3. Roma ni A, Ma rfella C, Scarpa A: Cell magnesium transport andhomeostasis: role of intracellular compartments. M iner Electrolyt eM etab1993, 19:282289.
4. Smith DL, Maguire ME: Molecular aspects of Mg2+ transport systems.M iner Electrolyte M etab1993, 19:266276.
5. Roof SK, Ma guire ME: M agnesium transport systems: genetics andprotein structure (a review). J Am Coll N utr1994, 13:424428.
6. Sutton RAL, Domrongkitchaiporn S: Abnormal renal magnesium han-dling. M iner Electrolyt e Metab1993, 19:232240.
7. de Rouffignac C, Ma ndon B, Wittner M, di Stefano A: Hormonal con-trol of magnesium handling. M iner Electrolyte Metab1993, 19:226231.
8. Whang R, H ampton EM, Whang DD : Ma gnesium homeostasis andclinical disorders of magnesium deficiency. Ann Pharmacother1994,28:220226.
9. McLean RM : M agnesium and its therapeutic uses: a review. Am J M ed1994, 96:6376.
10. Abbott LG, R ude RK: Clinical manifestations of magnesium deficien-cy. M iner Electrolyt e Metab1993, 19:314322.
11. Al-G hamdi SMG , Cameron EC, Sutton RAL: Magnesium deficiency:pathophysiologic and clinical overview. Am J Kid Dis1994, 24:737752.
12. Na dler JL, Rude RK: Disorders of magnesium metabolism.
Endocrinol M etab Clin North Am1995, 24:623641.
13. Kayne LH, Lee DBN : Intestinal magnesium absorption.M iner
Electrolyt e M etab1993, 19:210217.
14. Roth P, Werner E: Intestinal absorption of magnesium in man. Int J
Appl Radiat Isotopes1979, 30:523526.
15. Fine KD, Santa Ana CA, Porter JL, Fordtran JS: Intestinal absorption
of ma gnesium from food and supplements. J Clin I nvest1991,
88:396402.
16. di Stefano A, Ro inel N, de Rouffignac C , Wittner M: Transepithelial
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.
17. Nadler JL, Buchanan T, Natarajan R, et al.: Magnesium deficiency
produces insulin resistance and increased thromboxane synthesis.
H ypertension1993, 21:10241029.
18. Ryzen E, Elbaum N, Singer FR, Rude RK: Parenteral magnesium tol-
erance testing in the evaluation of magnesium deficiency. Magnesium1985, 4:137147.
19. Oster JR, Epstein M: M ana gement of magnesium depletion. Am J
N ephrol1988, 8:349354.
20. Physici ans Desk Reference(PDR). Montvale, NJ: Medical Economics
Compa ny; 1996.
References