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EFFECT OF THE ANTHYPEPTENSIVE
DRUGS (ALPHA TETHYDOPA, MODURETIC, AND HYDRALLAZINE) ON BLOOD PRESSURE AND
CONTRACTIONS OF SOCIAL, POTASSIUM, AND CALCIUM IONS IN BLOOD AND URINE OF
HYPERTENSIVE PATIENTS FOLLOWING SUBACUTE TREATMENT
TABLE OF CONTENTS
TITLE PAGE
AUTHOR’S
DECLARATION
SUPERVISOR’S
DECLARATION
DEDICATION
ACKNOWLEDGEMENTS
CONTENTS
ABSTRACT
CHAPTER ONE: INTRODUCTION
1.1 HYPERTENSION
1.2 ANTIHYPERTENSIVE DRUGS
1.3 OBJECTIVES OF STUDY
1.4 CHAPTER TWO : METHODOLOGY
2.1 MATERIALS
2.2 METHOD
PATIENTS
SAMPLE ANALYSIS
CALCULATIONS
CHAPTER THREE RESULTS (INCLUDING GRAPHS)
3.1 THE EFFECT OF
ANTIHYPERTENSIVE DRUGS ON THE BLOOD TRESSURE OF HYPERTENSIVE
PATIENTS
3.2 THE EFFECT OF
ANTIHYPERTENSIVE DRUGS ON SODIUM ION CONCENTRATIONS IN THE BLOOD AND URINE OF
HYPERTENSIVE
PATIENTS
3.3 THE EFFECT OF
ANTIHYPERTENSIVE GRUGS ON POTASSIUM ION CONCENTRATIONS IN THE BLOOD AND URINE
OF HYPERTENSIVE
PATIENTS
3.4 THE EFFECT OF
ANTIHYPERTENSIVE DRUGS ON CALCIUM ION CONCENTRATIONS IN THE BLOOD AND URINE OF
HYPERTENSIVE PATIENTS
CHAPTER FOUR: DISCUSSION
CHAPTER FIVE: SUMMARY
REFERENCES
ABSTRACT
The effect of the antihypertensive drugs, namely,
alpha –methyldopa, moduretic and hydralazine on blood pressure and blood and
urine concentrations of the elctrolytes, namely, sodium, potassium and calcium
of hypertensive patients was studied. Blood pressure was recorded by auscultory
method. Sodium and potassium concentrations were measured with flame photometer
while calcium was measured by colorimetric method. The hypertensive patients
consisted of inpatients and outpatients. For in-patients, drug administration
was daily for two weeks while it was three weeks for out-patients. Blood
pressure and electrolyte concentrations were measured every 4 days for
in-patients and weekly for out-patients. It was found that
1. Blood pressure of patients
consistently reduced after administration of alpha-methyldopa and moduretic.
Hydralazine, moduretic and alphamethydopa, however, caused greater blood
pressure reduction;
2. An increase in urinary
sodium excretion and potassium retention following administration of moduretic
and alpha-methyldopa correlated with the drug-induced blood pressure reduction;
3. The initial decrease and
later rise in calcium concentrations noticed in the blood and urine after
therapy did not correlate with the drug induced electrolyte concentrations were
less than those observed with the in-patients. The results suggest that
(1)
Combination of drugs with different mechanisms of action is
justifiable in anti-hypertensive therapy;
(2)
Increased urinary sodium excretion and potassium retention
may be relevant in the anti-hypertensive effect of moduretic and
alpha-methyldopa; and
(3)
Patient education on the need for compliance with drug
prescriptions may be important for the management of hypertensive
out-patients.
CHAPTER ONE
INTRODUCTION
1.1
HYPERTENSION
Blood pressure is the force exerted by the blood
against any area of the vessel wall (Guyton, 1981). The blood pressure (usually
measured in millimetres of mercury, mmHg) in the body needs to be maintained within
the normal range so that blood will adequately perfuse the tissues and organs
of the body supply them with enough nutrients. The systolic blood pressure of a
normal young adult (70kg) is about 120 mmHg while the average diasto0lic blood
pressure is 80 mmHg (Guyton 1981) that is mean arterial blood pressure of 93
mmHg (diastolic pressure plus 1/3 (systolic pressure minus diastolic
pressure)).
When the
blood pressure is higher than the normal for a given young adult, the
individual is said to have high blood pressure or hypertension. In
hypertension, the diastolic blood pressure has been sued as an index of the
severity of hypertensive state because it is the major blood pressure in the
blood vessel walls when the heart is at rest. Further, it is the major blood
pressure that maintains a steady blood flow in the vessels and causes the
tissues and organs to be well perfused with blood.
Hypertension
may be mild (90-105mmHg diastolic blood pressure), moderate (105-130mmHg
diastolic blood pressure, severe (130-140mmHg diastolic blood pressure) or
hypertensive crises (diastolic blood pressure > 140mmHg). Based on aetiology,
hypertension may be essential or primary (absence of causal factors) or
secondary (presence of causal factors) (Swales 1979), Guyton, 1981; Katzung
1982; Keel and Neil, 1971). Essential hypertension may be benign (210/110 blood
pressure) or Malignant (210/110 – 260/150 blood pressure) (keel and Neil,
1971). Secondary hypertension may be caused by
1. Sodium and water retention
2. Excess vasoconstrictor
(angiotensin II) secretion.
3. Goldblatt hypertension
(renal ischaemia) (4) excessive aldosterone secretion (5) nervous disorders or
stress (6) toxaemia of pregnancy (7) monomine oxidase inhibitors (orams, 1971)
and (8) alcohol (Saunders, et al 1981; Mitchell et al, 1980).
Hypertension can result in
compensatory hypertrophy of arteries and arterioles (Folklow et al, 1973), left
ventricular hypertrophy, coronary arteriosclerosis, cerebral or renal vessels
haemorrhage (Guyton, 1981), optic disc oedema, optic nerve lesions (leading to
blindness), arteriolar spasm, arteriolar necrosis, papilloedema, heart failure
leading to death (kneel and Neil, 1971).
1.2 ANTI-HYPERTENSIVE AGENTS:
Anti-hypertensive agents include diuretics (such as
hydrochlorothiazide), alpha-methyl noradrenalin in central adrenergic neurons.
The alpha-methyl noradrenalin exerts agonistic action at alpha (1 & 2)
receptors in the central nervous system (Vasomotor center) and thus inhibits
sympathetic outflow which results in reduction of blood pressure via reduction
of peripheral vascular resistance and relaxation of the arterial vasulature
(Katzung 1982; Swales, 1979). Alpha-methyldopa has also been found to lower plasmarenin.
Most cardiovascular reflexes remained intact after administration of
alpha-methyldopa and blood pressure reduction was not markedly dependent upon
maintenance of upright posture. it reduced blood pressure and peripheral
resistance while cardiac output and renal blood flow were maintained (Safar et
al 1979); but Katzung (1982) reported that there was little change in heart
rate and cardiac output.
Owing to
extensive first-pass metabolism (primarily o-sulphate conjugation by the
gastrointestinal mucosa), the bio availability of alpha-methyldopa was low,
averaging 25% (Kwan et al 1976; Saavedra et al 1975; Katzung, 1982). Orally,
its maximum effect lasted up to 24 hours. About 2/3 of the drug that reached
the plasma was cleared by renal excretion. It had a t1/2 for 2 hour (kwan et al
1976; Barnett et al 1977; Katzung, 1982). Impaired renal function resulted in
reduced drug clearance (Myhre et al 1972; Katzung 1982).
Side and toxic
effects of alpha-methyldopa include salt and water retention (Schild, 1980).
Dry mouth, nasal stuffiness, drowsiness, impotence in some males (Glontz et al,
1968).
Drowsiness, vertigo, overt
sedation, psychic depression, extra-pyramidal sings, nightmares, lactation
associated with increased prolactin secretion, jaundice (Elkington et al, 1969;
Katzung, 1982).
Hydrallazine: Hydrallazine acts directly on the
arterioles to cause relaxation and decrease of blood pressure. The vascular
relaxation and decreased blood pressure elicited compensatory responses
mediated by baroreceptors and sympathetic nervous system, as well as renin,
angiotensin and aldosterone (Swales, 1969, Katzung 1982; Schild 1980).
Hydralazine is well-absorbed orally and rapidly metabolized
by the liver during the first pass, mainly by acetylation (Reidemberg et al,
1979). The bioavailability was low (averaging 25%) and variable among
individuals. Simultaneous ingestion of food and hydralazine increased the bio
availability of the frung (Melander et al 1977).
Side-effects include headache, nausea, anorexia, palpilations,
weating, flushing, salt (Na+) and water retention, nasal congestion,
iacrimation, paraesthesia, oedema, tremor, muscle cramps and urticarial
(Swales, 1969; Katzung, 1982)
Hydrochlorothiazide: Hydrochlorothiazide exerts
its diuretic effect largely by inhibiting tabular reabsorption of sodium and
water at the early segments of distal convoluted tubule of the kidney nepron
(Tsaifan, 1981; Katzung, 1982). Friedman et al (1960) also observed that
hydrochlorothiazide exerted its anti-hypertensive effect by reducing vascular
muscular tone resulting from reduced intracellular sodium content. Hydrochlorothiazide
caused secretin of potassium in exchange for sodium, resulting in increased
potassium excretion at distal tubule (Giebisch, 1976; shild, 1980). It was
reported also that hydrochlorothiazide reduced renal excretion of calcium
(Edwards et al, 1973; Katzung 1982). However, Tsaifran (1981) has observed that
it induced calciuresis by inhibiting calcium reabsorption, calcuresis was
reduced by increased renal tabular calcium reabsorption.
Hydrochlorothiazide also inhibited tabular secretin of uric
acid because it competed with it for secretion (Katzung, 1982).
When given orally, hydrochlorothiazide is absorbed from the
gastrointestinal tract. The drug was shown to have a high degree extent by the
renal tabules. Hydrochlorothiazide underwent active secretion in the proximal
tabule and was excreted within 3 to 6 hours.
Toxic effects include weakness, paresthesias, potassium
depletion and metabolic alkalosis, impaired carbohydrate tolerance,
hyperuricemia and hyperlipidemia, hyponatremia and allergic reactions
(christensson et al 1977; Dolley 1973; Katzung, 1982; steele et al 1977;
Linderman et al, 1976).
Amiloride: Amiloride, one of the potassium- sparring
diutics increases sodium loss and reduces potassium loss by a direct action on
ion transport in the renal distal tubule. Gatzy (1971) has shown that amiloride
inhibited secretion of potassium and thus indicated that it could cause
potassium retention.
About 15-26% of the drug is absorbed in the
gastrointestinal tract. After oral administration, its action on the kidney
reached a peak within about 6 hours and ceased within 24 hours (Mudge, 1980;
Laurence, 1980).
Its toxic effects include hyperkalaemia, muscle weakness,
adominal pain, stiffness, paraesthesia in the extremities, cardiac arrest and
increased secretion of Uvic acid (Bowman and Rand, 1980).
1.3: OBJECTIVES OF STUDY
As indicated above, the
anti-hypertensive agents under discussion have been reported to alter the
con-centration of important electrolytes such as sodium (Na+),
potassium (k+), and calcium (ca2+) tisaitan, 1981;
Katzung 1982; Schild, 1980; Giebisch, 1976; Gatzy, 1971). Moreover, skraball et
al (1981) had reported that a high potassium intake promoted sodium loss,
prevented rise in plasma catecholamines, increased baroreflex sensitivity and
then reduced diastolic blood pressure.
The present study was, therefore, carried out in order to
examine the relationship between the concentration of these electrolytes and
the changes induced in the blood pressure of hypertensive patients following
the administration of anti-hypertensive agents. It is hoped that the knowledge
gained in this study will shed more light on the mechanisms of action of these
drugs more light on the mechanisms of action of these and the causes of
hypertensive states.
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