الفهرس 
group OF SEVERE HYPERTENSION)يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
This work included 45 patients with essential hyper tension, (39) males and 6 females, their age
ranged from 40 to 67 years,while 20 normotensive subjects of the same age were considered as a
control group. The hypertensive patients were classified according to the level of their
diastolic blood pressure into three groGps: The mild hy- perte sion group ith diastolic
tlood press re 90
104 !!ll11Hg. The moderate ypertension grop with diastolic blood pressure 105 - 114 rnrrHg.
The severe !1ypertension group with diastolic blood pressure 115 mmHg (Kaplan,
1988).
The hyperte si e patients wer accide tly dis-
covered, or they stcpred reatme for at leas one mo th before examination. Patie ts also ere
free frc any meta- bolic absorbers o diseases t at a · a e= calci etabc-
lism. 7he follo i g labc atory proced res were do e to
both hypertensive and control groups:
(!) Total serum calcium level.
(2) Serum sodium and potassium.
(3) Blood urea and serum creatinine.
(4) Fasting blood sugar.
(5) Co plete uri e exa ination.
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The data were statistically analyzed,and it was found
that:-
(1) There was a slight increase in the mean serum calcium level in the hypertensive group
compared to the con- trol group. But there were 5 patients out of the hy- pertensive group who
showed a frank elevation of their mean serum calcium level to 11.28 mg/dl, compared to the
control group. This may be due to abnormalities in the hormones regulating calcimetabolism,
and probably due to deviations in the plasma renin ac tivity in essential hypertension.
It was hypothesized that deviations in plasma renin activity in patients with essential
hypertension, refl ct an altered steady-state distribution of cal cium between various
intracellular and extracelL.Jlar compartments, which may be due to primary defects in membrane
ion transport. Also the calci m regulating hormones, regulate The distribution of calcium
and magnesium between extracellular and intracellular com partments of many tissues.
The dietary calcium supplementation may either, lower blood pressure, predominantly in low
renin forms of hypertension, or may raise it in renin dependent forms of hypertension.
Therefore it ···ould be·w-ise to restrict dietary calcium sJpplements in patients ith
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high renin-activity-associate Wlth elevated serum ionized calcium.
(2) A significantly higher level of serum sodium was found in patients with essential
hypertension, compared to the normotensive control group. This may be due to a differently
in excreting sodium, as it was suggested that the primary abnormality ir. essential hyperten-
sio!1, is in the kidney ·,.;ith difficulty in sodium excre-:ic::. This =e ds oi c ease the
extracellular fl:. id ’,·oll:me, leading o t e 3.ppearar..ce o£ ::he
atriuretic hormone, hich inhibits a/K ATPase, in- fluencing membrane permeability, causing an
increase in the ir.”’:: acel:t.:la cor:secu.e:J::.lv
lea5i g to ar. i:J= ase ln evas- calar tor.e, and hypertensio:J develops. The ir:creased
sodium a d · >o·a-:er conter’.ts i:1side Lf:e .:ascGlar SiTIOOt::
::-:’’.JScle c-::lls, i creases t e pe pteral resista!12e a d tte blood press e increases.
.;lso t’le
diet ric i sodim may be a ca se or
serum sod.1urn.
(3) Potassium levels were found to be significant lower in patients it essential hypertension,
included in this v>ork compared ’:0 the control group. This state of relati\ e
hypo-potasse::”.ia ir: these ratients,
reflect a condition of defective electrogenic ping
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of sodium and potassium, as it was found that the fluxes of sodium and potassium, across
the cellular membrane, are increased in hypertension, and the in- crease in K+ turn over-rate
precedes the development of hypertension. This also increases the vascular tone. Also the
cause of this relative hypokalemia, may be the limited dietary intake of potassium; ar:d
T...;as r:ot due to potassi depletion ind·.1ced by
diure ics as aties werethe=apy o o e no -
The real cause of this hypokalemia should be ose ly
.:=.:::·eci c.2 .l \-
effe:::: c:’.
le>Jel in blcod. So here is a increase i so i and
:::-a.lci’J.:T’.,
·.-.;crk.
The above e tio ed finai ;s observed i c r ork, ma· elp to identi the benefic a.l role of
calc c a nel blc:::..Cers,
treatrne t of hyper e sio , aim i this studv.
Furthermore, increasir:g potassium supplementation in the diet by 60 - 70 meq/day, may show an
antihypertensive effect through direct vasodilator effect of K, suppressic of plasa renin
activity, increased ri ary kallikrein, anj po-:assium in:J.uced sodium diuresis (Young et al.,
1976).
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from the above mentioned observation, we can con- elude that a few hypertensive patients, may
have an in- creased total serum calcium level, increased serum sodium and decreased serum
potassium. Also, these hypertensive patients need to be more investigated as regards the cal-
cium regula ing hormones, plasma renin activity and serum ionized calcium level, to identify,
which type of the hy- pertensive patients may or may not benefit from oral cal-
ci m supple entation.
•:estigated.
Also aljostercne level should be in-
It was suggested that patients with low renin ac tivity and low serum ionized calcium, show a
great hypoten- si e res;c se o oral 2alciu s pple e a ic , ’...::-:i.le -:hcse
·,·ith ’:tig’”t renin and hi::Jh ser•cc:E ior.ized cal:::ium le·.cel, :c1ay
have a pressor respor.se ’:O calcium suprlementatio!”l. .n.lso,
patients wi h low renin and lower ionizej calcium profile,
channel blocker ifedipine, hile ose ith higt re i are
less responsive to nifedipine (Austin et al., 1979}.
Finally, we recommend:-
(1) Sodi:nn restriction in hypertensi·.·e patients.
(2) Increased potassium supplementation in the diet of the hypertensive patients because, the
relative lower potassium level in some hypertensive patients ay be
d e to deficient potassi intake in t e diet.
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(3) Oral ca’+ supplemental in patients with hypertension with low renin activity and low ionized
Ca++.