AMERICAN
Vol. 229,
JOURNAL
OF PHYSIOLOGY
No. 5, November
1975.
Printed
in U.S.A.
Effect of parathyroid
hormone secretion
reabsorption
by the proximal tubule
EDWARD
Department
G. SCHNEIDER
of Physiology, Center for the Health
Sciences, University
dog micropuncture;
phosphate
plasma
ionized
calcium
REGULATION
of anion
reregulator
of isotonic
reabhas recently
been suggested
by Knox and Davis ( 12). The possible role of parathyroid
hormone
as a regulator
of not only phosphate
reabsorption
but also sodium
reabsorption
by the proximal
tubule
has
been supported
by micropuncture
studies
from
several
laboratories
which have shown that the infusion
of exogenous bovine
parathyroid
hormone
inhibits
sodium
reabsorption
by the proximal
tubule
(I, 17). At present,
however, no experimental
evidence
has been presented
which
demonstrates
that selective
increases
in endogenous
parathyroid
hormone
secretion
can affect sodium
reabsorption
by the proximal
tubule.
The purpose of this study was to determine
if a selective
increase
in the endogenous
secretion
of parathyroid
hormone could produce
an inhibition
of sodium
reabsorption
by the proximal
tubule of the dog.
THE
IMPORTANCE
0F
excretion;
HORMONAL
absorption
as a physiological
sorption
by the proxirnal
tubule
METHODS
Three
groups
eight
unilaterally
of experiments
were performed:
thyroparathyroidectomized
group
v-mw
1,
of Tennessee, Memphis,
Tennessee 38163
dogs received
an infusion
of a sodium
citrate,
sodium
chloride solution
into the blood supply of the remaining
parathyroid
gland;
group II, five acutely
TPTX
dogs received
an infusion
of a sodium
citrate,
sodium
chloride
solution;
and group III,
seven dogs with intact
parathyroid
glands
received
an infusion
of a sodium
chloride
solution.
All dogs were fed a standard
pellet diet providing
approximately
30 meq of sodium
per day. The dogs were
allowed free access to water; food was withheld
on the day
of the experiment.
The dogs were anesthetized
with pentobarbital
(30 mg/kg),
a tracheotomy
was performed,
and
the dogs were prepared
for clearance
and micropuncture
as previously
described
( 18).
In group I, immediately
following
removal
of the right
parathyroid
and thyroid
glands, the left carotid
artery was
occluded
beyond
the origin
of the thyroid-parathyroid
artery. A 23-gauge
needle connected
to an infusion
pump
was inserted
into the left carotid
artery 5-8 cm below the
origin of the thyroid-parathyroid
artery, and a 0.5-ml/min
infusion
of 0.9 % NaCl was initiated.
After three successive
15-min
clearance
periods
had been obtained,
the carotid
arterial
infusion
was changed
to a 5-mg sodium
citrate per
minute
per kilogram
body weight
infusion
made isotonic
by the addition
of sodium
chloride
and adjusted
to pH 7.4.
Sixty
minutes
later
three
additional
15-min
clearance
periods were performed.
In group II experiments
the dogs were bilaterally
thyroid
parathyroidectomized
2 h before starting
the initial
clearance measurements.
These dogs were then treated
in an
identical
manner
to group I except that the sodium
citrate
solution
was infused into the left jugular
vein. In group III
experiments
the dogs received
an infusion
of isotonic
sodium
chloride
solution
(0.5- 1 .O ml/min)
throughout
the
experimental
protocol.
During
the clearance
measurements,
micropuncture
samples were obtained
from late proximal
tubule
segments
using the recollection
micropuncture
technique.
Late proximal tubule
segments
were identified
by the injection
of
small nonocclusive
oil droplets
as previously
described
for
this laboratory
(15). Tubule
fluid samples were collected
at
a rate which was sufficient
to collect all the volume
flow
at the puncture
site and hold a column
of stained
castor
oil distal to the puncture
to prevent
retrograde
flow ( 18).
The volume
of the tubule fluid sample was measured
with a
with
a radioactive
micropipette
which
was calibrated
tracer. The single-nephron
filtration
rate (snfr) was calculated from the expression
snfr = V, X (TF/P)r,
where V,
is the volume
collected
per minute
and the (TF/P)
rn is
1170
Downloaded from http://ajplegacy.physiology.org/ by 10.220.32.246 on April 2, 2017
SCHNEIDER,
EDWARD
G. EJect of parathyroid hormone secretion on
sodium reabsorption by the proximal tubule. Am. J. Physiol.
229(5) :
1170-l 173.
1975.-To
determine
if an increase
in the endogenous secretion of parathyroid
hormone could decrease sodium
reabsorption
by the proximal
tubule,
the ionized calcium
concentration
of blood perfusing
the parathyroid
gland of eight unilaterally thyroid parathyroidectomized
dogs (TPTX)
was reduced
by infusion
of an isotonic sodium
citrate
plus sodium
chloride
solution
into the blood supply
of the parathyroid
gland. The
fractional
clearance
of phosphate
increased
significantly
(+9.3
k 2.8 ml/min
per 100 ml GFR),
while fractional
sodium
reabsorption
by the proximal
tubule decreased
(- .06 h .02; P <
.025). In seven normal control dogs that received isotonic sodium
chloride
infusion,
neither fractional
sodium reabsorption
by the
proximal
tubule nor the fractional
clearance
of phosphate
was
significantly
altered. In five bilaterally
TPTX
dogs that received
a sodium
citrate
plus sodium
chloride
infusion,
sodium
reabsorption
by the proximal
tubule
was not significantly
altered.
There were no significant
changes in glomerular
filtration
rate
or renal plasma flow in any of these groups. The data demonstrate
that alterations
in endogenous
parathyroid
hormone
secretion
can play a significant
role in the regulation
of sodium reabsorption
by the proximal
tubule.
on sodium
PTH
SECRETION
AND
PROXIMAL
SODIUM
REABSORPTION
study were done in duplicate
in three
different
serum
dilutions.
In tra-assay
and in terassay
variations
were 12
and 15 %, respectively.
The average for a variable
during
the initial
clearance
periods
was compared
by the Student
I test for paired
comparison
to the average obtained
for that variable
during
the experimental
clearance
periods.
Differences
between
groups
were compared
by the Students
t test for group
comparison.
The data are expressed as the mean value zt 1
SE.
RESULTS
A summary
of the plasma calcium
and plasma phosphate
data for all dogs is presented
in Table
1. Following
the infusion of a sodium
citrate
solution
into the blood supply
of the parathyroid
gland (group I), arterial
ionized
calcium
concentration
obtained
from
the left carotid
artery
was
significantly
less ( - -88 + -31 mg/ 100 ml ; P < .05) than
the ionized
calcium
concentration
obtained
from femoral
arterial
blood.
The femoral
arterial
ionized
calcium
concentration
was not significantly
changed
(.OO =t .03 mg/ 100
ml) (Table
1) following
this infusion.
Total plasma calcium
was not significantly
changed in group I (+. 3 1 & .16 mg/ 100
ml) ; however,
this change
in total
plasma
calcium
was
significantly
greater
(P < .05) when compared
to the
change in total plasma
calcium
obtained
in dogs receiving
only an infusion
of sodium
chloride
(group 111). Following
the infusion
of a sodium
citrate solution
into acutely TPTX
dogs (group Ir), total
plasma
calcium
concentration
decreased significantly
(- -31 * .lO mg/loo
ml; P < .05).
The plasma
phosphate
concentrations
in, the three groups
of dogs during
the hydropenic
periods were not significantly
different.
Plasma
phosphate
concentration
did not change
following
the sodium
citrate infusion
in group I or following
the sodium
chloride
infusion
in group III. However,
plasma
phosphate
concentration
increased
significantly
( + 1.3 &
.4 mg/lOO
ml; P < -05) in the TPTX
dogs (group II) following
the sodium
citrate
infusion.
Associated
with the
infusion
of sodium
citrate into the blood supply of the parathyroid
gland
(group I), serum
immunoreactive
PTH
increased 26 A 8 &eq/ml
(n = 3), which was significantly
greater
(P < -05) than the change
in serum iPTH
(-3
in TPTX
dogs receiving
* 2 pl-eq/ml;
n = 2) obtained
the same infusion
of sodium
citrate.
Serum
iPTH
concenTABLE
~__I
1. Summary
______~
of plarma
-~.~
calcium
and phosphate
______.
data
Plasma
Phosphate,
mg/lOO
ml
II
Grout I, n = 8
Intact + Na
citrate
Group II, n = 5
TPTX
+ Na
citrate
Group III, n = 7
Intact + NaCl
E
9.2
Ifs.1
9.5
h.3
9.7
Zk.1
9.5
Ik.2
H
4.03
zk.10
E
H
Femoral
Carotid
4.03
Zt.09
3.17*
AZ.35
E
5.4
It.3
5.6
h.4
9.4*
k.1
5.6
zk.5
6.9*
zk.4
9.4
It.3
6.3
zt.4
6.3
AZ.4
Values
are means & SE. H, bydropenic
periods;
E, experimental periods.
* P < .05 cornDared
to the hvdroDenic
Deriod.
Downloaded from http://ajplegacy.physiology.org/ by 10.220.32.246 on April 2, 2017
the ratio of inulin
concentration
in tubule
fluid to that in
plasma.
The concentration
of inulin
in the tubule fluid was
determined
in duplicate
by a microfluorometric
method
(19). Fractional
reabsorption
(FR) of sodium
and water
by the proximal
tubule
was calculated
from the following
expression : FR
= 1 (P/TF)
Ina Blood
samples
were
collected
at the midpoint
of the 15-min
urine
collection
periods.
Inulin
in plasma
and urine was measured
by the
anthrone
method.
The PAH
concentration
in plasma
and
urine was measured
by the method
of Harvey
and Brothers
(10). Renal plasma flow was calculated
from the clearance
and extraction
of PAH.
Sodium
and potassium
concentrations in plasma
and urine were measured
by flame photometry.
Phosphate
in plasma
and urine was measured
by
the method
of Young
(20). Calcium
and magnesium
in
plasma
and urine
were measured
by atomic-absorption
spectroscopy.
In group I peripheral
and carotid
arterial
blood for ionized
calcium
were collected
into a syringe and then injected
into
S-ml
Vacutainers
(Becton-Dickinson,
Rutherford,
N. J.)
containing
143 PU heparin.
Plasma was withdrawn
anaerobically into a tuberculin
syringe through
the rubber stopper
of the Vacutainer
after contrifugation
at 3,000 rpm for
10 min. For measurements
of ionized
calcium
in plasma,
the Orion
flow-through
calcium-activity
electrode
(16)
was used with
the following
modifications:
I> standards
were prepared
in Vacutainers
containing
the same amount
of heparin
as the samples.
2) No trypsin or triethanolamide
was added to the standards,
which were prepared
weekly,
and 3) the membrane
was primed
by pooled normal
plasma
before the daily
standard
curve was run. Plasma
pH was
measured
by a microelectrode
and a standard
pH meter.
In three dogs in group I and two dogs in group 11, arterial
blood
was obtained
during
the control
and experimental
periods
for measurement
of serum immunoreactive
parathyroid
hormone
(iPTH)
concentration.
The
techniques
of measurement
of serum iPTH
were the same as those
reported
in a previous
publication
(2). The antiserum
used
in the present
studies was termed
CHl 2M (chicken
antibovine
PTH)
and was described
in the previous
report.
In the present
studies,
a crude saline extract
of pooled
normal
dog parathyroid
glands was used as a standard
in
all radioimmunoassays.
This
was assigned
an arbitrary
value of 1,000 Ill-eq/ml,
and immunoassay
curves produced
with this standard
were superimposed
on curves produced
with multiple
dilutions
of a serum obtained
from a dog made
1311~
chronically
hypocalcemic
with
citrate
infusions.
labeled
bovine
PTH
was used in assays as the labeled
hormone
species. Antiserum
CHlZM
reacts with synthetic
bovine
PTH
l-34 (Beckman
Bio-products)
almost
as well
as with bovine
PTH
l-84 and, therefore,
recognizes
the
biologically
active region of the PTH’molecule.
Sera from
normal
dogs consistently
decreased
the ratio of antibody
bound to free 1311-labeled
bovine
PTH
(B/F ratio)
by 3050 %, whereas
sera from
hypoparathyroid
dogs did not
alter
this ratio
significantly,
indicating
that iPTH
was
being measured
and not some nonspecific
effect of serum
on the immune
system. In order that this potential
problem
could
be circumvented,
we used hypoparathyroid
dog
serum in assays as a blank and made corrections
for small
nonspecific
changes in the B/F ratio as has been described
(12). All measurements
of serum
iPTH
in the present
1171
E. G. SCHNEIDER
1172
3. Summary of proximal
tubule micropuncture data
--.- - _~-_~_____~
_- _._. -_____
~~----_
-~ _____-_____-__
---
TABLE
Dog No.
E
H
E
H
-_-25
*2
25
*2
.30
sf.02
E
H
I -.--_-~__________
Group I (n = 8)
.32
0.6
0.6
zt.03
A.2
*.2
E
H
E
~___~~_____._
___.
0.6
*.2
0.5
*.l
14
*3
23*
*3
1.3
3~5
1.1
h.6
11
&3
13
A3
Group II (n = 5)
30
*3
30
*3
.32
zt.03
.33
LO2
0.6
rt.4
Group III
0.8
A.3
26
&6
.24
AZ.03
.29
A.05
1 .l
*.3
Fractional
__--H
_____
Reabsorption
E
~
Single-Nephron
Filtration
Rate, nl/min
-. H
E
~.___
- -~. ~~___
__
Group I
I
2
3
4
5
6
7
8
6
5
3
5
6
5
3
6
.49
.45
.25
A-0
.43
.59
.21
.41
A-0
.38
.25
.32
.42
.45
.21
.34
113
86
58
88
102
93
80
71
85
81
56
92
72
71
A-0
.43
A0
.36
.45
130
80
82
108
98
117
75
80
122
95
A-0
.32
.21
.36
.33
.23
.47
75
89
67
89
92
59
55
78
84
79
89
97
51
61
(n = 7)
21
24
*3
*4
-_ .~
Values
are means & SE. H, hydropenic
periods;
E, experimental periods.
* P < .025 compared- to the hydropenic
period.
29
zt6
No. of
Tubules
0.8
*.2
1 .O
*.3
0.8
*.1
DISCUSSION
The present study was designed
to examine
the effect of
a selective increase in endogenous
PTH secretion
on proximal sodium
reabsorption
in the dog. Several
observations
indicate
that the infusion
of sodium
citrate
into the parathyroid
gland increased
the endogenous
secretion
of PTH.
It has been established
that PTH
secretion
is inversely
correlated
with the plasma
ionized
calcium
concentration
rather
than total
plasma
calcium
concentration
(8, 15).
Documentation
of the perfusion
of the parathyroid
gland
was obtained
bythe injection
of lissamine
green dye through
the infusion
catheter
and directly
observing
the perfusion
of the thyroid
and parathyroid
glands
in several of the
dogs.
Following
the sodium
citrate
infusion
in dogs with inin total plasma
caltact parathyroid
tissue, the increases
cium concentration
and in phosphate
excretion
are consistent with
an increase
in the secretion
of PTH
(11).
9
IO
II
I2
13
5
4
3
6
5
.39
.47
.32
.41
.46
Group III
14
15
16
17
18
19
20
4
5
3
2
4
4
4
.39
.24
.33
.34
.32
.17
.50
Mean data
Group I
39
.4ozt.o4
.34&03”
Group II
23
.41+ .02 .41zk .Ol
Group III
26
.33zt.O4
.33rt.o3
- -_- .--- ---Values are means rf= SE. H, hydropenic
period;
period.
* P < .05 compared to the hydropenic
85&7
loo*9
75*6
79sft8
98zk9
77zk6
E, experimental
period.
Furthermore
75 min following
the start of the sodium
citrate infusion
in dogs with intact parathyroid
tissue there
was a consistent
increase in serum iPTH
concentration
in
the three dogs in which that variable
was measured.
Because the samples for iPTH
were obtained
75 min following
the start of the sodium
citrate
infusion,
the magnitude
of
the change
in plasma
iPTH
concentration
probably
does
not accurately
reflect
the maximum
change
in serum
iPTH
concentration.
Fischer et al. (8) have demonstrated
that the maximum
increase in serum iPTH
concentration
occurs within 4 min of a fall in plasma ionized
calcium
and
that after 15 min the serum iPTH
concentration
declines
somewhat
from the maximum
level, even though
plasma
ionized
calcium
may continue
to decrease.
Consequently,
lowering
of the plasma
ionized
calcium
concentration
perfusing the parathyroid
gland in the present study caused a
significant
increase in the secretion of parathyroid
hormone.
Several
observations
suggest that following
the sodium
citrate
infusion
into dogs with intact
parathyroid
tissue,
the small but consistent
inhibition
of fractional
sodium
reabsorption
by the proximal
tubule
was caused by an increase in endogenous
PTH
secretion.
In the absence
of
intact parathyroid
tissue, a sodium
citrate infusion
did not
cause a detectable
inhibition
of proximal
sodium
reabsorption
or an increase in phosphate
excretion.
That acute
thyroparathyroidectomy
prevented
an increase
in plasma
Downloaded from http://ajplegacy.physiology.org/ by 10.220.32.246 on April 2, 2017
tration
in the hydropenic
periods
averaged
41 A 12 pleq/ml
for the three dogs in group I and 29 & 11 pl-eq/ml
for two dogs in group II.
A summary
of the clearance
data is presented
in Table 2.
NO significant
changes in glomerular
filtration
rate, filtration fraction,
or the fractional
clearance
of sodium
or calcium occurred
in any of the groups. The fractional
clearance of phosphate
increased
9.3 & 2.8 ml/min
per 100 ml
GFR
(P < .025) following
the sodium
citrate
infusion
in
group I. The fractional
clearance
of phosphate
was not
significantly
changed in either group II or group III.
A summary
of the micropuncture
data is presented
in
Table
3. Following
the infusion
of sodium
citrate
solution
(group I), fractional
sodium
reabsorption
by the proximal
-0.058
rt 0.18 (P < .025) which
is
tubule
decreased
equal
to a 14% inhibition
in sodium
reabsorption.
This
change
in proximal
sodium
reabsorption
was not associated with any significant
change
in single-nephron
filtration rate. In neither
group II nor group III dogs were there
any significant
changes in fractional
sodium
reabsorption
by the proximal
tubule
or in the single-nephron
filtration
rate.
Group II
PTH
SECRETION
AND
PROXIMAL
SODIUM
1173
REABSORPTION
crease
phosphate
excretion,
while
Cuche
(4) could
find
no
the previous
observation
that infusion
of exogenous
PTH
inhibits
proximal
sodium
reabsorption
and extends
these
observations
by demonstrating
that the endogenous
release of PTH
can influence
sodium
reabsorption
by the
proximal
tubule.
The importance
of PTH
in mediation
of the decrease in
sodium
reabsorption
by the proximal
tubule
following
infusion of hyperoncotic
albumin
solution
has recently
been
demonstrated
by Knox
et al. ( 13). Preferential
expansion
of the plasma
volume
failed
to produce
an inhibition
of
sodium
reabsorption
by the proximal
tubule
if the endogenous
release of PTH
was prevented.
The endogenous
release of parathyroid
hormone
was shown to mediate
the
inhibition
of sodium
reabsorption
by the proximal
tubule
in the presence
of preferential
plasma
volume
expansion.
The present
study supports
this conclusion
and further
demonstrates
that the endogenous
release of PTH
can inin anihibit
sodium
reabsorption
by the proxi ma1 tubule
mals without
preferential
pl asma volume expansion.
The
author
gratefully
acknowledges
the
technical
assistance
of
Theresa
Berndt,
Joann
Caron,
Sally
Gleason,
and Karen
Drake
and
the secretarial
assistance
of Wanda
Cross.
The
author
also thanks
Dr. C. R. Arnaud,
Mayo
Clinic,
for performing
the immunoassay
for parathyroid
hormone.
This
investigation
was supported
in part
by Public
Health
Service
Grant
HL- 16658.
E. G. Schneider
is an Established
Investigator
of the American
Heart
Association.
Received
for
publication
29 October
1974.
REFERENCES
1. AGUS,
2. S., J. B. PUSCHETT,
D. SENSEKY,
AND h/I. GOLDBERG.
Mode
of action
of parathyroid
hormone
and
cyclic
adenosine
3’) 5’-monophosphate
on renal
tubular
phosphate
reabsorption
in the dog. J. C/in. Invest.
50: 617-626,
1971.
2. ARNAUD,
C. D., H. S. TSAO, AND T. LITTLEDIKE.
Radioimmunoassay
of human
parathyroid
hormone
in serum.
J. Clin.
Invest.
50: 21-34,
1971.
3. BRUNETTE,
M., AND M. ARAS. A microinjection
study
of nephron
permeability
to calcium
and
magnesium.
Am.
J. Physiol.
221:
1442-1448,
1971.
4. CUCHE,
J.-L.
Absence
of direct
effect
of plasma
ionized
calcium
on fractional
excretion
of sodium
and
phosphate
(Abstract).
Federation
Proc. 33 : 325, 1974.
5. DIBONA, G. F. Effect
of hypercalcemia
on renal
tubular
sodium
handling
in the rat. Am. J. Physiol.
220: 49-53,
197 1.
6. EDWARDS,
B. R., R. A. L. SUTTON,
AND J. H. DIRKS.
Effects
of
calcium
infusion
on renal
tubular
reabsorption
in the dog.
Am.
J. Physiol.
227:
13-18,
1974.
7. EISENBERG,
E. Effects
of serum
calcium
level
and
parathyroid
extracts
on phosphate
and calcium
excretion
in hypoparathyroid
patients.
J. Clin. Invest.
44: 942-946,
1965.
8. FISCHER,
J. A., U. BINSWANGER,
AND J. W. BLUM.
The
acute
parathyroid
hormone
response
to changes
in ionized
calcium
during
phosphate
infusion
in the cow.
European
J. C/in.
Invest.
3: 151-155,
1973.
9. GLORIEUX,
F., AND C. R. SCRIVER.
Loss of a parathyroid
hormone-sensitive
component
of phosphate
transport
in X-linked
hypophosphatemia.
Science 175 : 997- 1000,
1972.
10. HARVEY,
R. B., AND A. J. BROTHERS.
Renal
extraction
of paraaminohippurate
and creatinine
measured
by continuous
in vivo
sampling
of arterial
and
renal-vein
blood.
Ann.
NY
Acad.
Sci.
102: 45-54.
1962.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
KLEEMAN,
C. R., S. G. MASSRY,
AND J. W. COBURN.
The clinical
physiology
of calcium
homeostasis,
parathyroid
hormone,
and
calcitonin.
Calif.
Med.
114: 16-43,
1971.
KNOX,
F. G., AND B. B. DAVIS.
Role of physical
and neuroendocrine
factors
in proximal
electrolyte
reabsorption.
Metabolism
23: 793-803,
1974.
KNOX,
F. G., E. G. SCHNEIDER,
L. R. WILLIS,
J. W. STRANDHOY,
C. E. OTT, J.-L.
CUCHE,
R. S. GOLDSMITH,
AND C. D. ARNAUD.
Proximal
tubule
reabsorption
after
hyperoncotic
albumin
infusion:
role of parathyroid
hormone
and dissociation
from
plasma
volume.
J. Clin. Invest.
53 : 50 l-507,
1974.
LAVENDER,
A. R., AND T. N. PULLMAN.
Changes
in inorganic
phosphate
excretion
induced
by renal
arterial
infusion
of calcium.
Am. J. P/z-ysiol. 205 : 1025-1032,
1963.
LYNCH,
R. E., E. G. SCHNEIDER,
J. W. STRANDHOY,
L. R. WILLIS,
AND F. G. KNOX.
Effect
of lissamine
green
dye on renal
sodium
reabsorption
in the dog. J. A/$.
Physiol.
35: 169-17
1, 1973.
MOORE,
E. W. Ionized
calcium
in normal
serum,
ultrafiltrates,
and
whole
blood
determined
by
ion-exchange
electrodes.
J.
C/in. Invest 49: 3 18-334,
1970.
SCHNEIDER,
E. G., J. W. STRANDHOY,
L. R. WILLIS,
AND F. G.
KNOX.
Relationship
between
proximal
sodium
reabsorption
and
excretion
of calcium,
magnesium
and
phosphate.
Kidney
Intern.
4: 369-376,
1973.
SCHNEIDER,
E. G., R. E. LYNCH,
L. R. WILLIS,
AND F. G. KNOX.
Single
nephron
filtration
rate
in the dog.
Am. J. Physiol.
222:
667-673,
1972.
VUREK,
G., AND S. PEGRAM.
Fluorometric
method
for the determination
of nanogram
quantities
of inulin.
Anal.
Biochem.
16: 409417, 1966.
YOUNG,
D. S. Improved
method
for the automatic
determination
of serum
inorganic
phosphate.
J. Clin. Pat. 19: 397-399,
1966.
Downloaded from http://ajplegacy.physiology.org/ by 10.220.32.246 on April 2, 2017
PTH concentration
is supported
by finding
a small decrease
in plasma
PTH
concentration
following
the infusion
of
sodium
citrate
in the two dogs in which that variable
was
measured.
Additionally,
the small but significant
decrease
in total plasma
calcium
concentration
and the significant
increase in plasma
phosphate
concentration
are consistent
with a decrease
in plasma
PTH
concentration.
The inhibition
of proximal
sodium
reabsorption
was not associated with
any detectable
alteration
in whole-kidney
or
single-nephron
glomerular
filtration
rate or in the filtration
fraction
for the whole kidney.
The magnitude
of the inhibition
of proximal
sodium
reabsorption
is similar
to that
obtained
in a previous
study following
the infusion
of
exogenous
bovine parathyroid
hormone
( 17).
It is unlikely
that a small increase in total plasma calcium
caused either the inhibition
of proximal
sodium
reabsorption or the increase in urinary
phosphate
excretion.
Several
investigators
(3, 5, 6) have shown that large increases (6-14
mg/ 100 ml)
in plasma
calcium
concentration
cause a
small inhibition
in sodium
reabsorption
by the proximal
tubule.
However,
the inhibition
of proximal
sodium
reabsorption
following
the infusion
of sodium
citrate into the
blood supply of the parathyroid
gland was not associated
with a statistically
significant
increase in either total plasma
calcium
or ionized
plasma
calcium
concentration.
Thus,
it is unlikely
that changes in plasma calcium
concentration
contributed
to the observed
inhibition
of sodium
reabsorption
by the proximal
tubule.
Eisenberg
(7) reported
that prolonged
infusion
of calcium
solution
in hypoparathyroid
patients
produced
increases in phosphate
excretion
;
other authors
have reported
conflicting
findings.
Lavender
and Pullman
( 14) and Glorieux
and Striver
(9) found
that acute increases in plasma
calcium
concentrations
de-