Hemodynamic Effects of Alterations
in Potassium
MARK S. PALLER, M.D.,
AND STUART L. LINAS,
M.D.
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SUMMARY Potassium is the major intracellular cation. Despite this fact, the systemic and renal
hemodynamic effects of alterations in either serum K or in total body K are only partially understood.
In isolated preparations acute K excess causes vasodilation while acute K deficiency results in vasoconstriction. Although chronic K excess may decrease arterial pressure in experimental models of
hypertension, no definitive conclusions can be stated on the effect of K excess in hypertensive patients.
In normotensive animals, chronic K depletion is associated with decreased systemic vascular resistance and increased renal vascular resistance. Although a number of studies have shown that K
depletion ameliorates experimental hypertension, no definitive conclusions can be stated on the effect
of K depletion in hypertensive patients. The vasodilatory effect of K depletion appears to be a direct
effect on vascular smooth muscle since it is associated with an increase in total body Na as well as an
increase in cardiac output and in renin and arginine vasopressin levels. Although renin levels are
increased in K deficient rats to a value comparable to Na-depleted rats, angiotensin antagonism
results in a substantially smaller decrease in arterial pressure than in Na-depleted rats (II ± 1.6 vs 24
± 3.4 mm Hg, p < 0.01). This relative resistance to the pressor effect of angiotensin also results in a
blunted pressor sensitivity to exogenous angiotensin II. Since changes in K balance appear to have a
major effect on the control of hemodynamics, further studies are warranted to determine whether
alterations in K balance would be useful in the treatment of hypertension.
(Hypertension 4 (supp HI): HI-20-III-26, 1982)
KEY WORDS • experimental hypertension
vasoconstriction • vasodilation
• renin-angiotensin
P
•
Hemodynamic Effects of Potassium
OTASSIUM is the major constituent cation of
all cells. In view of this fact, it is striking that
there have been so few studies on the hemodynamic effects of pertubations in total body K. In this
brief review, we will outline the current information on
this topic and consider several questions: 1) What are
the hemodynamic consequences of both K excess and
of K deficiency? 2) Are there differences between
acute changes in K concentration and chronic changes
in K balance? 3) What mechanisms are involved in
these hemodynamic effects of K? In particular, are
there accompanying changes in Na balance and in the
activity of endogenous pressor hormone systems or are
the hemodynamic changes a direct result of K on the
vascular smooth muscle cell?
Potassium Excess — Acute
Many investigators have demonstrated that the infusion of small quantities of K into isolated limbs or
arteries from normotensive animals results in vasodilation. 1 ^ For example, Overbeck and Clark4 infused KG
into the hindlimbs of normotensive, renal hypertensive, and genetically hypertensive rats. While all three
groups of animals had a substantial decrease in vascular resistance, the decrease in resistance in normotensive and genetically hypertensive rats was much greater than in rats with renal hypertension (14 vs 7 mm Hg/
ml/min). Similar infusion studies have been performed
in patients with essential hypertension.5 Although both
normotensive and hypertensive subjects had a vasodilator response following the administration of KG in
quantities that increased the venous K content to 7
mEq/liter, limb resistance remained substantially
greater in hypertensive subjects. Since the vasodilatory effect of K administration can be demonstrated in
isolated preparations, it is caused by a direct effect of K
on arterial smooth muscle cells rather than by changes
From the Department of Medicine. University of Colorado.
Health Sciences Center, Denver, Colorado.
Supported by National Institutes of Health Grants AM261O56
and AM07135.
Address for reprints: Dr. Stuart L. Linas, Department of Medicine, Denver General Hospital, 750 Cherokee Street, Denver.
Colorado 80204.
1-20
III-2I
POTASSIUM AND HEMODYNAMICS/Pa//<?r and Unas
in either sodium (Na) balance or in pressor hormone
activity. In studies of isolated perfused limbs by Chen
et al., 6 K-induced vasodilation was prevented or reversed when oubaine, an inhibitor of Na-K-ATPase,
was added. These investigators postulated that the vasodilator action of K was the result of stimulation of
membrane Na-K-ATPase activity, which resulted in
membrane hyperpolarization and relaxation of vascular smooth muscle.
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Potassium Excess — Chronic
In 1928 Addison7 reported that the administration of
K could lower blood pressure (BP) in humans. Moreover, he postulated that the reason for the high incidence of hypertension in the United States was related
to the North American diet, which tended to be higher
in Na and lower in K than in other parts of the world
where hypertension was substantially less prevalent.
Since this description, other investigators have also postulated that the relatively low K content of the North
American diet may be a cause of hypertension.8"15
There are a number of animal studies that have demonstrated that the administration of very large quantities of K could substantially blunt the hypertensive
effect of an extremely high Na diet.8"10 In 1972, Dahl
and his associates9 performed a very interesting study
demonstrating that even small increases in K intake
resulted in a decrease in blood pressure in hypertension-prone rats fed a high Na diet (fig. 1). In this study
rats were fed a 4.5% NaCl diet with varying concentrations of KCl. As the K content of the diet was increased
from a diet of normal K content (Na/K ratio of 10) to a
diet of high K content (Na/K ratio of 1), systolic BP
fell remarkably in these animals despite the high Na
intake. Moreover, even smaller increases in dietary K
(Na/K ratio of 2 or 3) caused a lowering of systolic
blood pressure.
There have been animal studies demonstrating the
protective effect of K on other experimental forms of
hypertension. For example, Suzuki et al." studied the
effect of adding 0.5% KCl to the drinking water of rats
with two-kidney, one clip hypertension. Whereas systolic pressure reached a level of 180-200 mm Hg in
water-drinking rats, systolic pressure was only 140—
150 mm Hg in K-drinking animals. In association with
amelioration of hypertension, there was a marked increase in urinary Na and water excretion. In addition,
the increase in PRA which is characteristic of twokidney, one clip hypertension was partially attenuated
in K-loaded rats. Although the authors postulated that
the hypotensive effect of K administration was due to
the decrease in PRA and the marked natriuresis and
diuresis observed in K-loaded rats, it is also possible
that the effect was due to a direct vasodilatory effect
of K.
The mechanism of the hypotensive effect of K administration in hypertensive rats is not clear. For example, it has not been determined whether the decrease
in blood pressure is caused by a decrease in cardiac
output or in systemic vascular resistance. Moreover, it
is not known whether the hypotensive effect is due to K
180
MOLAR
No/K
170
160
E
150
Q.
CO
i 140
130
120
- 4
no
100
2
3
4
5
6
7 8 9 10
MONTHS ON DIET
II
12
FIGURE 1. Effect on BP of different dietary Na/K molar ratios
in hypertension prone rats. All six diets had a 4.5% NaCl but
each differed in KCl concentration. (Reproducedfrom the Journal of Experimental Medicine, 1972, vol 136, p 318, by copyright permission of The Rockefeller University Press.)
administration per se or to the changes in Na balance or
in pressor hormone activity that accompany the administration of K. In this regard, the administration of KCl
results in a negative external Na balance. Young et
al.12 have studied both normal dogs and adrenalectomized dogs maintained on fixed quantities of both
gluco- and mineralocorticoids. When K intake was
increased from 30 to 200 mM per day, both groups of
animals went into negative Na balance and had a reduction in 22Na space after 6 days of the high K diet.
Moreover, adrenalectomized dogs became hypotensive because of greater Na loss and contraction of
extracellular fluid volume most likely due to the inability to increase aldosterone secretion. A similar effect of
K-loading on Na balance has also been demonstrated
in adrenalectomized humans.13 In addition to altering
Na balance, the administration of K results in a decrease in activity of renin and angiotensin II but an
increase in aldosterone in both experimental animals
and humans.l4- '5 In summary, the hypotensive effect of
K may be multifactorial but at the present time it has
never been dissociated from the natriuretic effect of K
administration.
There have also been studies exploring the role of K
excess in the treatment of hypertensive humans. Probably the studies most often mentioned are those of
Kempner16 employing the rice-fruit diet as the sole
therapy of hypertension. Whereas the low Na content
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of the diet is well-recognized, its normal-to-increased
K content is frequently overlooked as a possible cause
of the hypotensive effect of the diet. Several British
studies have reexplored the effect of dietary K supplementation in the treatment of hypertension.17"19 In one
of these studies,18 subjects were maintained on their
usual Na intake or on a diet that was mildly Na restricted and was supplemented with 100 mM of KC1 per
day. There was no effect of K administration on the
blood pressure of normotensive individuals. In contrast, K supplementation initially lowered blood pressure in hypertensive subjects ( - 8 . 9 ± 11.2/-6.4 ±
9.4 mm Hg, p < 0.05). However, this effect was not
sustained, and by 12 weeks the blood pressure of hypertensive subjects was not significantly different from
their baseline. Moreover, since the study period included a diet restricted in Na as well as enriched in K,
it is not possible to determine whether the changes in
pressure were caused by an excess of K or a decrease in
Na.
In summary, whereas the hypotensive effect of K
administration has been clearly demonstrated in hypertensive rats, it has not been conclusively demonstrated
in hypertensive humans. Further investigation is clearly warranted.
Potassium Deficiency — Acute
Many studies have demonstrated that perfusing isolated vessels, limbs, and organs from normokalemic
animals with hypokalemic solutions results in vasoconstriction.20"23 For example, when Anderson et al.22
decreased the K concentration of the blood perfusing
the gracilis muscle of the dog by placing a dialyzer on
the arterial side of the muscle, vascular resistance increased by 10% when K concentration fell by 40%.
The mechanism of the local vasoconstrictor effect of
acute hypokalemia is independent of both changes in
Na balance and in pressor hormone activity since it can
be demonstrated in isolated perfused arterial preparations. It is likely to be a direct effect of vascular smooth
muscle, but the precise biochemical events accompanying hypokalemia remain to be defined.
Potassium Deficiency — Chronic
Chronic sustained dietary K deficiency has been
demonstrated to result in a decrease in systemic vascular resistance in all but one study24 in which systemic
TABLE 1.
Rat
group
K replete
(n = 12)
K deplete
(n = 8)
p value
III, HYPERTENSION,
VOL.
4, No 5,
SEPTEMBER-OCTOBER
hemodynamics have been determined.25-27 For example, Galvez et al.26 produced K deficiency in dogs over
several weeks and then measured hemodynamic parameters in conscious restrained animals. There was a
33% decrease in vascular resistance. Mean arterial
pressure remained unchanged as cardiac output increased to the same extent that vascular resistance fell.
Of further interest was the observation that the vasodilatory effect of K occurred despite an increase in total
body Na and an increase in plasma volume of 40%.
In the rat, Freed and Friedman28 originally demonstrated that K deficiency resulted in hypotension. We
have also studied the effects of K deficiency on systemic hemodynamics in the rat.27 For these studies, K
was withheld from the diet. Control rats were fed an
identical diet to which K had been added. Aside from
K, the sodium, calcium, magnesium, chloride, and
phosphorous contents of the two diets were comparable. Animals were studied after 14-17 days of K restriction at which time the plasma K was 2.3 mEq/liter
compared to 4.1 mEq/liter in control rats. Muscle and
kidney K content was decreased by about 18%. Hemodynamic studies were performed by the microsphere
methodology in conscious restrained animals.
Table 1 demonstrates the effect of K deficiency on
systemic and renal hemodynamics. There was a slight
decrease in mean arterial pressure. Just as in the K
deplete dog, systemic vascular resistance was decreased by about 30% while cardiac index was increased but, in contrast to the dog, not quite enough to
maintain arterial pressure. Moreover, as previously
shown by Sealey et al.,' 4 balance studies demonstrated
the rats to be in positive Na balance, and this increase
in total body Na was reflected by an increase in plasma
volume (4.08 ± 0.2 vs 3.5 ± 0.1 ml/100 g body
weight, p < 0.05). In summary, therefore, despite an
increase in total body Na and in plasma volume, chronic dietary K deficiency results in a decrease in systemic
vascular resistance and, in the rat, mean arterial
pressure.
What about the effects of K deficiency in hypertension? As already noted, Addison7 and others8""-15"19
have suggested that one possible cause of the higher
incidence of hypertension in the United States is that
the North American diet tends to be low in K. There
are, however, a few studies in both man and animals
that suggest that K deficiency may actually lower
Effect of K Depletion on Systemic and Renal Hemodynamics in the Conscious Rat
RBF
(ml/min-g-')
RVR
(mm Hg/ml-
±0.2
3.60
17.8
±0.8
29.6
±0.2
< 0.001
6.64
1982
MAP
(mm Hg)
CI
(ml/min-kg"1)
119.6
±1.8
338
±21
±0.8
108.1
±3.5
408
±16
< 0.001
< 0.01
< 0.05
SVR
(mm Hg/mlmin~ '-kg" 1 )
0.37
±0.03
0.27
±0.01
< 0.01
RBF = renal blood flow; RVR = renal vascular resistance; MAP = mean arterial pressure; CI = cardiac index; and
SVR = systemic vascular resistance.
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POTASSIUM AND HEMODYNAMICS/Pa//er and Unas
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blood pressure in hypertension. Perera29 studied the
effect of dietary K deficiency in five patients with
essential hypertension. In this study patients were
limited to 25-30 mEq K per day. All five patients had a
hypotensive response to K deficiency. The mean decrease in blood pressure was 15/9 mm Hg, and the
blood pressure returned to baseline soon after the Kdeficient diet was discontinued.
There are two animal studies evaluating the effects
of K deficiency on renal hypertension. Rosenman et
al. 30 studied rats with one-kidney, one figure-8 hypertension. Animals were placed on a diet of normal K
content (0.3%) or on one of two K-deficient diets:
0.03% or 0.006% K. As seen in figure 2, when K was
removed from the diet of rats with established hypertension, systolic blood pressure decreased after a 4week delay. Fisher and Funckes31 have demonstrated a
protective effect of K deficiency in rats with two-kidney, one clip hypertension. In these studies, animals
were clipped after 6 weeks of a K-deficient diet. Hypertension did not develop in animals maintained on
the K-deficient diet. In contrast, animals became hypertensive within 1 week of initiation of a normal K
diet.
In preliminary studies, we too have found that K
deficiency markedly alters the natural history of twokidney, one clip renovascular hypertension. Following
placement of a 0.25 mm silver clip on the left renal
artery, rats were placed on a normal K diet (n = 9) or a
K-deficient diet (n = 16). In rats maintained on the
normal K diet, systolic blood pressure increased to 133
± 5 mm Hg (mean ± SEM) 7 days after clipping and
reached a value of 149 ± 4 mm Hg by 21 days. In
contrast, in K-deficient rats systolic blood pressure
only reached a level of 112 ± 4 mm Hg (p < 0.001)
after this 3-week period.
In summary, chronic dietary K deficiency results in
vasodilation. Further studies are warranted to determine the hemodynamic effects of chronic K deficiency
in experimental models of hypertension. Moreover, it
is important to recognize that all of these studies have
been performed in animals that were at least 15% Kdepleted. This corresponds approximately to a 500
mEq deficit in humans, i.e., moderate-to-severe K
deficiency.
In addition to altering systemic hemodynamics, dietary K deficiency results in profound changes in renal
hemodynamics. In the presence of this very remarkable systemic vasodilation, renal vascular resistance
was increased and renal blood flow decreased by about
40% in K deplete rats (table I). 27 We have recently
completed studies on the mechanism of the increase in
renal vascular resistance.27 Since angiotensin levels are
increased in the K-deficient rat, the role of angiotension as a renal vasoconstrictor was determined. The
administration of either saralasin or teprotide lead to a
substantial increase in renal blood flow in K deficient
animals (fig. 3). However, since renal blood flow remained less than in control rats, it appeared that there
was a second renal vasoconstrictor present. In recently
published studies, Beck et al.32 have demonstrated that
thromboxane production is increased in kidneys from
K-deficient rats. Since thromboxane is a vasoconstric-
|
1 K Deplete
ES5 K Deplete plus Saralasin
B8H K Replete plus Saralasin
Renal
Blood Row 4
(ml/min-gm-1)
GROUP m
(0.3% K)
p<.01
2-
I
I K Deplete
E§3 K Deplete plus Medofenamate
B888I K Replete phis Medofenamate
p<.O1
—GROUPn
(0.03 % K)
"* GROUP I
(0.006 %K)
I 2 3 4 5 6 7
NUMBER OF WEEKS
FIGURE 2. Effect of potassium deprivation upon blood pressure of hypertensive rats. (Reproduced from the American Journal of Physiology, 1953, vol 175, p 386, by copyright permission of The American Physiological Society.)
Renal
Blood Flow
(ml/min-gnr1)
P<.01
FIGURE 3. The effect of saralasin and sodium medofenamate
on renal blood flow in K depleted and K repleted rats. (Reproduced from Kidney International, 1982, vol 21, p 757, by copyright permission of the publisher.)
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PERSPECTIVES IN HYPERTENSION
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tor product of prostaglandin metabolism, the role of
thromboxane as a vasoconstrictor in K deficiency was
determined by utilizing prostaglandin cyclooxygenase
inhibitors and a selective thromboxane synthetase inhibitor. Figure 3 demonstrates that cyclooxygenase inhibition with meclofenamate resulted in a substantial
increase in renal blood flow in K deficient animals.
Identical results were obtained utilizing indomethacin
and the selective thromboxane synthetase inhibitor,
imidazole. Moreover, none of these agents altered systemic or renal hemodynamics in K-replete animals.
Finally, because neither angiotensin antagonism nor
prostaglandin inhibition alone decreased renal vascular
resistance to levels sufficient to restore renal blood
flow, studies were performed in which angiotensin and
prostaglandins were both inhibited. Utilizing indomethacin and either saralasin or teprotide, renal blood
flow was restored to normal values in K-deficient rats.
Thus, we concluded that the increase in renal vascular
resistance in K-deficient rats was caused by both angiotensin II and a vasoconstrictor product of prostglandin endoperoxide metabolism, namely, thromboxane.
While the mechanism of renal vasoconstriction during K deficiency has been determined, the mechanism
of systemic vasodilatation is not known. The decrease
in systemic vascular resistance is of particular interest
since it occurs in the setting of an increased cardiac
output and activation of endogenous pressor systems.
In this regard, plasma renin activity is increased,14 and
in preliminary studies we have found that arginine
vasopressin levels (3.5 ± 0.2 vs 2.4 ± 0.2 pg/ml, p
< 0.02)33 are increased in K-deficient rats. Moreover,
it is well recognized that K deficiency results in an
increase in total body Na.26-27-34
While there are no studies that have determined the
reason for the increase in vasopressin in K deficiency,
a number of possibilities seem likely. Although it is
possible that K deficiency per se results in increased
hormone biosynthesis, a more likely possibility is that
the vasodilation of K deficiency results in activation of
arterial baroreceptors. Moreover, since K deficiency
results in a renal concentrating defect,35 it is possible
that a subtle increase in plasma osmolality may lead to
the osmotic stimulation of vasopressin release.
Two recent studies have examined the mechanism
of increased renin secretion in the K-deficient rat. The
three major intrarenal receptor mechanisms that control renin release are a vascular receptor, a renal tubular receptor (macula densa), and a beta adrenergic receptor. Luke et al.36 have concluded that a renal tubular
mechanism mediates the increase in renin secretion. A
pivotal part of these studies was the observation that
the administration of sodium chloride suppressed renin
secretion in control rats but failed to suppress renin
secretion in K-deficient animals. In earlier studies
these investigators had shown that chloride transport
was critical in suppressing renal tubular mediated renin
release and that choride transport may be decreased in
K deficiency. Thus, they concluded that the failure of
sodium chloride to suppress renin was caused by an
inability to transport chloride in K-deficient animals.
III,
HYPERTENSION, VOL
4, No 5,
SEPTEMBER-OCTOBER
1982
In recent studies we concluded that the renal vascular receptor mediated the increase in renin.37 For these
studies, the isolated perfused kidney was utilized since
ex vivo renal perfusion allows renin release to be studied in the absence of renal nerves and circulating factors such as catecholamines, which are known to directly increase renin secretion. Since renin production
was increased in K-deficient perfused kidneys, stimulation of the renal beta receptor could be eliminated as
the cause of hyperreninemia. Moreover, the increase
in renin was associated with an increase in renal vascular resistance and a decrease in urine flow rate. Hence
it was possible that either a vascular or a tubular
mechanism could have accounted for the increase in
renin. To determine if the decrease in distal nephron
fluid delivery contributed to the increase in renin, delivery was enhanced by decreasing the albumin concentration of the perfusate. Just as Luke et al.36 had
shown, renin levels could not be suppressed by increasing distal nephron fluid delivery. Of importance,
however, was the fact that in association with the enhanced delivery, vascular resistance remained increased in K-deficient kidneys. Moreover, when distal
nephron fluid delivery was eliminated by perfusing
with hyperoncotic albumin, a maneuver that eliminates glomerular filtration, renin levels remained increased and perfusion flow rate decreased in K-deficient kidneys. Since renin production by K-deficient
kidneys was greater than renin production of control
kidneys, even in the absence of distal nephron fluid
delivery, the mechanism of hyperreninemia in the Kdeficient perfused kidney occurred independent of
changes of macula densa fluid delivery or transport.
To determine whether the increase in renal vascular
resistance could have mediated the increased renin,
nonfiltering kidneys were perfused with papaverine, a
dilator of vascular smooth muscle. As seen in figure 4,
papaverine caused a decrease in vascular tone in Kdeficient kidneys. Moreover, the decrease in vascular
tone was accompanied by a decrease in renin levels in
K-deficient kidneys to values observed in control kidneys. Since papaverine had no direct effect on renin
secretion, we concluded that the renal vascular receptor mediated the increased renin production in the Kdeficient perfused kidney.
Although there is an increase in pressor hormone
levels in K deficiency, the role of these hormones in
the support of blood pressure has only recently been
studied. Table 2 demonstrates the effect of angiotensin
antagonism with saralasin in control rats and in rats
maintained on a Na- or K-deficient diet for 14 days.
Angiotensin inhibition resulted in a minimal depressor
effect in control rats. As expected, Na-deficient rats
had a very large decrease in mean arterial pressure. Kdeficient animals had a substantially smaller decrease
in pressure despite basal renin levels that were comparable to those of Na-deficient animals. Thus, while
angiotensin clearly supports mean arterial pressure in
Na deficiency, it has a relatively modest pressor role in
K deficiency. This relative resistance to the pressor
effect of angiotensin in K deficiency has been known
POTASSIUM AND HEMODYNAMlCS/Pa//er and Unas
T
40
-r
30
Perfusion
Flow Rate
(ml/min/g)
p<.OI
20 10 -
a
tm
•
NORMAL K
0 PAPAVEPWE
E 3 H OEFICIENr
7
6
r ^ v l f DEFICIENr
LiiJ
0 PAPAVE PINE
Renin
5 Activity
(ng A,/ml/hr)4 •
3
l
i
p<.OI
P<.OI
p<.OI
2
I
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FIGURE 4. 77?e e^i?c7 of papaverine on perfusion flow rates
and on renin activity in K depleted and K repleted isolated
perfused kidneys. (Reproduced from the Journal of Clinical
Investigation, 198!, vol 68, p 347, by copyright permission of
The Rockefeller University Press.)
for many years and results in blunted pressor sensitivity to exogenous angiotensin II.38
Table 2 also demonstrates the effect of the administration of phenoxybenzamine, an alpha-adrenergic
blocking agent. The hypotensive effect of alpha-adrenergic inhibition was comparable in both control and Kdeficient rats. Moreover, since pressor sensitivity to
norepinephrine is preserved in K-deficient animals,39
the results suggest that the decrease in pressor sensitivity to angiotensin is not caused by a generalized defect
in smooth muscle reactivity but rather to a specific
defect in angiotensin sensitivity. The results of recently completed studies are consistent with the conclusion
that an alteration in the binding affinity of angiotensin
II smooth muscle receptors mediates the decreased
pressor sensitivity to angiotensin in K deficiency.40
Conclusions
The hemodynamic effects of alterations in serum K
or in total body K content are only partially understood. In isolated preparations, acute K excess results
in vasodilation, while acute K deficiency results in
vasoconstriction. Chronic K excess results in a decrease in arterial pressure in hypertensive animals; no
definitive conclusions exist on the effect of K excess in
hypertensive man. The mechanism of the decrease in
arterial pressure in hypertensive animals appears to be
multifactorial, but at the present time it has never been
dissociated from the natriuretic effect of K administration. Chronic K deficiency results in a decrease in
arterial pressure in normal animals and may also decrease blood pressure in hypertensive animals. The
mechanism of vasodilation appears to be a direct effect
on the vascular smooth muscle since it occurs despite
an increase in total body Na, renin, and arginine vasopressin. Further studies are warranted to determine
whether alterations in total body K could be linked to
the higher incidence of hypertension in the United
States. Studies are also indicated to determine whether
dietary or pharmacological manipulation of K would
be useful in the treatment of hypertension.
Acknowledgments
Vicki Van Puttcn provided technical assistance and Carolyn Bignail provided secretarial assistance.
References
TABLE 2. Effect ofK Depletion on Plasma Renin Activity and on
the Depressor Response to Teprotide and Phenoxybenzamine
Rat
group
Renin
(ng Al/ml/hr)
2.2 ± 0.7
(n = 8)
Reduction in
MAP with
teprotide
(mm Hg)
5.2 ± 1.9
(n = 7)
6.8 ± 0.8t
24.4 ± 3.4t
Na deplete
(n = 7)
(n = 6)
8.5 ± 0.9t
II ± 1.6**
K deplete
(n = 8)
(n = 7)
Data are expressed as the mean ± SEM.
*p < 0.05 vs control.
tp < 0.01 vs control.
tp < 0.01 vs Na depleted.
Control
Change in
MAP with
phenoxybenzamine
(mm Hg)
10.6 ± 1.9
(n = 5)
8
9.
12.1 ± 2.5
(n = 7)
111-25
10
11
Emanuel DA. Scott JB. Haddy FJ: Effect of potassium on
small and large blood vessels of the dog forelimb. Am J Physiol 197: 637, 1959
Konold P, Gebert G, Brecht K: The effect of potassium on the
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Overbeck HW: Vascular responses to cations, osmolality. and
angiotensin in renal hypertensive dogs. Am J Physiol 223:
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Overbeck HW, Clark DWJ: Vasodilator responses to K+ in
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Overbeck HW, Derifield RS. Pamnani MD. Sozen T: Attenuated vasodilator responses to K+ in essential hypertensive
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Hemodynamic effects of alterations in potassium.
M S Paller and S L Linas
Hypertension. 1982;4:III20
doi: 10.1161/01.HYP.4.5_Pt_2.III20
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