A COMPARATIVE STUDY OF THE EFFFECTS OF OXPRENOLOL, ATENOLOL AND PROPRANOLOL ON SOME PHYSIOLOGICAL PARAMETERS IN HEALTHY MAN.
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A
COMPARATIVE STUDY OF THE EFFFECTS OF OXPRENOLOL, ATENOLOL AND PROPRANOLOL ON
SOME PHYSIOLOGICAL PARAMETERS IN HEALTHY MAN.
TABLE OF CONTENTS
DECLARATION
DEDICATION
ACKNOWLEDGEMENT
LIST
OF TABLES
LIST
OF FIGURES
ABSTRACT
CHAPTER ONE:
1.1 INTRODUCTION AND
LITERATURE REVIEW
1.2 MECHANISM OF ACTION OF
BETA-ADRENOCEPTOR BLOCKERS
1.3 OXPRENOLOL
1.4 ATENOLOL
1.5 PROPRANOLOL
1.6 SCOPE OF THE PROJECT
CHAPTER TWO
2.1
MATERIALS
2.2
DRUGS
2.3
METHOD
2.4
STATISTICAL ANALYSIS
CHAPTER THREE
3.0
RESULTS
3.1
BLOOD PRESSURE
3.2
HEART RATE
3.3
EXERCISE-INDUCED TACHYCARDIA
3.4
LUNG VOLUME
3.5
24-HOUR URINARY ELECTROLYTE OUTPUT
CHAPTER FOUR
4.1
DISCUSSION
4.2
CONCLUSION
REFERENCES
ABSTRACT
This project was intended
to study the effects of acute administration of 80mg propranolol retard on:
a.
Blood pressure and heart rate
b. Exercise-induced
tachycardia
c.
Lung volumes
d. 24-hour urinary
electrolyte output.
It was also intended to
compare the effects of these agents following acute administration, with place
to with a view to determining the physiological and biochemical changes
associated with the mechanism of action of these drugs in healthy man.
Six healthy normotensive medical students (all males)
aged 22-27 years and of mean weight, 68kg, took part in the study. The study was
single-blind. Each subject took in a randomised order either of the three drugs
or placebo and at least 7 days was allowed between re-investigation of any
subject.
The results show that none of the three drugs produced a
significant reduction in blood pressure, when compared with placebo. Also no
significant reduction in supine heart rate observed. Atenolol and propranolol
produced a significant reduction of erect heart rate (p<0.01) whereas
oxprenolol did not. All the three drugs caused a significant reduction of
post-exercise heart rate (p<0.02). None of the drugs significantly affected
the forced vital capacity (P>0.05) while all the drugs caused modest
alterations in the 24-hour urinary electrolyte output. The resulting indicate
that beta-adrenoceptor blockers may not be effective on acute administration in
blocks. However, these findings require further investigation in an appropriate
patient population.
CHAPTER ONE
1.1
INTRODUCTION AND
LITERATURE REVIEW
Norepinephrine,
epinephrine and other catecholamines can cause either excitation or inhibition
of smooth muscle, depending on the site, the dose, and the catecholamine
chosen. Norepinephrine is the most potent excitatory catecholamine and has
correspondingly low activity as an inhibitor. Epinephrine is relatively potent
as an excitor and as an inhibitor of smooth muscles. On the basis of such
observations, Ahlquist (1948) propounded a hypothesis that two types of
adrenoceptors exist: the alpha (ϕ) and the beta (β) adrenoceptors. This
classification of receptors has been corroborated by the findings that certain
drugs selectively antagonize the alpha-adrenoceptors whereas some other agents
selectively antagonize the beta-adrenoceptos. The alpha-adrenoceptors are
divided into two types: alpha-1 and alpha-adrenoceptors. (Starke, 1977). There
are drugs that antagonize the activities of these adrenoceptors either
selectively or non-selectively. Hence we have drugs that antagonize both
alpha-1 and alpha -2 adrenoceptors (eg. Phenoxybezamine) and those that act
only on alpha-1 adrenoceptors (eg. Prazosin). Starke et al 1975; langer 1977).
The beta-adrenoceptor antagonists (beta-blockers) may be divided into beta-1
selective antagonists (eg. Atenolol) and non-selective antagonists with
affinity for the both beta-1 and beta-2 adrenoceptors (eg. Propranolol) (Levy
and wilkenfeld, 1969). There are also drugs that antagonize both the alpha and
beta-andrenoceptors (eg. Labetalol). (Brittain and Levy, 1976; Richards and prichads,
1978).
The first drug shown to produce a selective
blockade of beta-adrenoceptors was dichloroisoproternol (DC1) (Powell and
Slate, 1958). Studies with DC1 made a susbstantial contribution to the
understanding of effects mediated by berta-adrecoceptors, but a prominent
beta-receptor stimulant action; that is, it is a partial agonist. The initial
report of the hypotensive effect of beta-adrenoceptors blocking drugs appeared
in 1964 (Prichard). Pronethalol was
administered to some hypertensive patients and then to some normotensive
patients who were being treated for angina pectoris. A significant fall in
blood pressure was recorded after three months’ therapy. However, pronethalol
was withdrawn because of its carcinogenic effects in mice. These of propranolol
in hypertension was described later the same year.
The cardiselective or beta-1-adrenoceptor
antagonists include atenolol, and metoprolol. It is important to remember that
the selectivity of the beta-1-blockers is not absolute; larger doses of these
compounds will inhibit all beta-adrenoceptors (Prichard, 1978). The
non-selective beta-adrenoceptors antagonists include propranolol, nadolol,
oxprenolol, alprenolol, penbutolol, sotalol and timolol. The beta-blockers in
each group may exert two types of effects namely: membrane stabilizing activity
and intrinsic sympathomimetic activity.
It has been considered that large doses of
some beta-blockers have ‘direct depressing action’ (‘quinidine-like effect’,
membrane action’ local anaesthetic effect), on the heart in man. A membrane
action is seen with large doses in animals (Coltart, Gihson and Shand, 1971).
It however has no relevance to treatment of hypertension and is certainly not
responsible for the haemodynamic effects of beta-adrenoceptor antagonists since
no significant membrane stabilizing activity occurs with clinically effective
doses of beta-blockers. The quinidine-like effects of beta blockers appears to
contribute little to the treatment of cardiac arrhythmias. Effective
concentrations of propranolol in blood are below those that cause membrane
stabilization. In addition beta-blockers without this property are also
effective anti-arrythnic agents (Black and Prichard 1973; Shand, 1975).
The clinical significance of intrinsic
sympathomimetic activity (ISA) is controversial. From a theoretical point of
view it has been argued that the beta-blockers with ISA for example oxprenolol
and pindolol, may protect against development of cardiac failure (Imhof, 1976).
It has been shown, however, that in the treatment of hypertension and angina
pectoris, drugs weith ISA are as effective as beta-blockers without this
property, for example atenolol and propranolol (Harry, 1975; Prichard 1970;
Thadani et al, 1980). In healthy subjects ISA modified the haemodynamioc
response to beta-blockers, in that heart rate and cardiac output were less with
atendlol and propranolol than when beta-blockers with ISA were used (Svensen et
al 1980). Beta-blockers with ISA do not change the total peripheral resistance
index. Beta-blockers without ISA, on the other hand, increase the total
peripheral resistance, reflecting peripheral vaso-construction (Svendsen et al
1981) the receptors involve in this action are the peripheral
beta-2-adrenoceptors.
Occasionally today one talks of
the various genera tons of beta-blockers. The ratio of beta-1- to beta – 2
blocking potency has been calculated as well as the significance of intrinsic
sympathomitic activity or of membrane stabilizing effect. Some of these attempts
have demonstrated, to an extent, the superiority of one or the other
representative of the whole group in the treatment of high blood pressure.
1.2
MECHANISM OF ACTION OF
BETA-ADRENOCEPTOR BLOCKERS
The beta-adrenoceptor blocking drugs appear to lower the blood pressure
as a result of a variety of mechanisms involving beta-adrenoceptor blockade.
Blood pressure falls regardless of the presence or absence of the association
properties. There have a number of hypothesis to explain the hypotensive effect
of beta-asrenoceptor blocking agents, including a direct action on the central
nervous system (CNS), adrenergic neurone blockade, antirenin activity, an
increase of vasodilator blockade, anti-renin activity, an increase of
vasodilator prostaglandins, effects secondary to reduced cardiac output and
resetting of baroreceptors secondary to reduced pressor peaks from the
reduction in cardiac activity.
i.
Central nervous system
Some observation in
animals suggest a possible central mode of action. Intra-arterial injection of
propranolol into either the carotid or vertebral artery in the anaesthetized
dog produces a fall in blood pressure of more rapid onset than if administered
via the femoral artery (offerhaus and Van Zvrieten 1974). Several
beta-adrenoceptor antagonists (propranolol, atenolol, oxprenolol, pindolol,
practolol and sotalol) when injected into the cerebral ventricle of conscious
normotensive cats have been shown to produce a transient rise followed by a
fall in blood pressure (Day and Roach, 1974).
Some beta-adrenoceptor blocking drugs when
adminis tered systemically penetrate the CNS and concentrations rapidly achieve
a steady state. However, in cats, for example, there was no evidence of
accumulation in the cerebrosmial fluied following two weeks administration of
oxprenolol compared to acute administration (offerhaus and Van Zwieten, 1974).
Other experiments in cats using equivalent hypotensive doses of metoprolol and
atenolol have revealed up to a nine-fold higher concentration of metoprolol
compared to liquid insoluble atenolol (Offerhaus et al, 1975).
While beta-adrenoceptor drugs can influence
central sympathetic activity it is unlikely that this is the only explanation
for their anti-hypert4ensive action in man. Beta-adrenoceptor blocking drugs,
such as sotalol, that apparently do not cross the CNS still have an effective
antihypertensive effect in man.
ii. Adrenergic
neurone blocking action
The adrenergic neurone blocking effect that
has been observed in rats and rabbits has been found not only from racemic
propranolol but also with the d (+) isomer which is devoid of antihypertensive
effects in man. The fact that propranolol and other beta-adrenoceptor
antagonists reduced blood pressure in man without producing the postural
hypotension characteristic of the adrenergic neurone blocking drugs (Prichard
and Gillam 1969) also indicates that an adrenergic neurone inhibition is not
important.
iii. Renin
blocking activity.
Beta-adrenoceptor
inhibition lowers plasma renin in normotensives and hypertensive (Buhler et al
1972) although the beta-adrenoceptor stimulation is not the only factor
involved in renin release (Bravo et al 1974).
Buhler et al (1972) subdivided their
hypertensive patients prior to treatment into high, normal and low renin groups
according to their ambulant peripheral renin levels and daily urinary sodium
excretion. 540mg propranolol was given daily to all the patients. After a
week’s therapy it was found that the 12 high renin patients showed greatest
falls in blood pressure, the 14 low renin level patients failed to show a
significant fall in pressure while the 23 patients with normal renin levels had
intermediate falls of blood pressure. There was a good overall correlation
between the fall in blood pressure and plasma renin activity. Prepranolo,
exprenolol were studied in a further series of 137 patients (Buhler et al 1975)
and the results of the previous investigators (Burhler et al 1972) were
confirmed.
On the other hand, there is considerable
evidence against the effects on renin being the predominant mechanism of the
antihypertensive action of beta-blockers. Several investigators have failed to
find a relationship between the fall in blood pressure and pre-treatment levels
of plasma renin (Leonetti et al, 1975; Morgan et al 1975). Morgan et al (1975)
observed similar falls in blood pressure with low, normal and high renin
patients. Additionally, relatively small doses of propranolol which suppress
plasma renin levels have little effects on blood pressure. It has been
suggested that renin suppression may be important in lowering blood pressure when
beta adrenoceptor antagonists are given to patients taking vasodilators as they
do reverse the rise in renin which results from the ingestion of vasodilators
(Pettinger and Mitchell, 1976).
In conclusion, while the fall in blood
pressure in some patients with high renin levels may be due, at least in part,
to the antirenin activity of beta-blockers, overall, the present evidence
cannot be regarded as more thanindicating the possibility that the antirenin
activity of beta-blockers is the main mechanism of their antihypertensive
effect.
iv. effect
on plasma volume
Tarazi et al (1971) observed that
propranolol reduced plasma volume in a series of 14 hypertensive patients
although this failed to correlate with the fall in blood pressure. Blood
pressure fell in some patients without a fall in plasma volume. Julius et al (1972)
noted a fall in plasma volume after acute intravenous propranolol but as others
had shown before, blood pressure did not fall. Other investigators have found
an increase in plasma volume after the administration of beta-adrenoceptor
blocking drugs, propranolol 30mg a day increased plasma volume after one month
despite a fall in blood pressure `(Gordon 1976). Larger doses of propranolol (40mg
3 times daily) produced inconsistent effects with a fall in blood pressure in
seven (7) and no change or an increase in the remaining six (6) patients.
(Brave et al, 1975). The evidence therefore suggests that it is unlikely that
changes in plasma volume are of major importance in the hypotensive action of
beta-adrenoceptors antagonists.
Other mechanisms which have been proposed
for the action of beta-blockers include increase of vasodilator prostagladnins,
effects secondary to rediced cardiac output and resetting of barao-receptors
secondary to reduced pressor peaks from the reduction in cardiac activity.
The beta-blockers after a hesitating start
have now become first line drugs in the treatment of Caucasian hypertensive
patients and their use is continuing to increase. How they lower the blood
pressure is yet to be ascertained. Drugs with such varied actions, as beta-blockers,
may well lower blood pressure by more than more than one mechanism. In some
cases one of the many effects may be of overriding importance eg. Reducing
plasma renin in patients with high plasma renin level.
1.3
OXPRENOLOL
Oxprenolol is a non selective beta-adrenoceptor
antagonist. It exhibits intrinsic sympathomimetic activity (ISA) and also has a
considerable membrane stabilizing effect which in potency is about half of
lignocaine.
PHAMACOLOGICAL PROPERTIES:
Schlesinger and Barzilay (1980) working on the effect
of oxprenolol on patients with essential hypertension found that there was a
significant reduction in heart rate and systolic and diastolic blood pressure
in both supine and erect positions after treatment for 4 weeks. Also a
significant reduction in forced expiratory volume in second (FEV1) was observed
and this was due to the inhibition of bronchodialtion, (beta-2 effect) by
oxprenolol.
ABSORPTION, METABOLISM AND EXCRETION
Orprenolol is appreciably absorbed when taken orally.
Like propranolol, it is subject to first pass effect, hence its short
elimination half-life which is about 2 hours.
Oxprenolol is
considerably bound to plasma proteins. It is virtually completely metabolised
in the liver before excretioj in the urine as metabolites of less potency
compared to the parent drug.
TOXICITY & SIDE EFFECTS:
The minor
side effects of oxprenolol include nausea, voliting, dizziness, and mild
diarrhea. Owing to its effect on the bronchioles, exprenolol may precipitate
severe broncho constriction in predisposed patients. Hence it is contra
indicated in asthma patients.
THERAPEUTIC USES:
Oxprenolol is
used in the treatment of hypertension. Beta-blockers cause unwanted effects due
to alterations in peripheral blood flow. These have included an awareness of
cold limbs, an increase in intermittent claudication and peripheral gangrene
(Rodger et al 1975; Frohlich et al 1969; Simpson 1974; Vale and Jeffreys 1978).
There is evidence that this problem may be reduced by using oxprenolol instead
of propranolol (Roberts et al 1977). In a controlled trial designed to compare
the effect of oxprenolol and propranolol on resting foream blood (RFBF) when
administered acutely and chronically in patients with essential hypertension,
it was shown that a reduction in RFBF after acute administration and after 2
weeks therapy occurs with both drugs, the reduction being greater and more
prolonged with propranolol than with greater and more prolonged with
propranolol than with oxprenolol. It was also shown that total peripheral
resistance was not changed by oxprenolol whereas propranolol increased the
total peripheral resistance was not changed by oxprenolol whereas propranolol
increased the total peripheral resistance. It is likely that oxprenolol is
exerting a different effect because of its ISA either by direct stimulation of
the peripheral beta-adrenergic receptors or, reflex in consequence of tis
causing a lesser reduction of the cardiac output than propranolol (Malcolm 1982).
Hence it could be concluded that in hypertensive patients with peripheral
vascular disease, oxprenolol is safer milligram for milligram than propranolol.
Also in bradycardia and in situations in which a decrease in cardiac output is
inappropriate or if the beta-blocking effect is required during physical and
psychic stress, a beta-blocker with ISA might be advantageous.
1.4 ATENOLOL:
Atenolol is a
selective beta-1 – adrenoceptor antagonist which is mainly used in the
treatment of hypertension. Atenolol lacks both intrinsic sympathomimetic
activity (ISA) and membrane stabilizing activity. Its chemical structure is
shown in fig. 1.
PHARMACOLOGICAL PROPERTIES
Fuller and
Vallance (1982) found that atenolol reduced FEV1 and blood pressure in
normotensive subjects after acute administration. Leoneti et al (1982) were
able to show that blood pressure decrease was very significant during the first
day of hypertensive therapy with atenolol and was uncahged after seven and
ourteen days of chronic treatment. The degree of blood pressure reduction was
very similar in both supine and erect positions. The bradycardiac effect was
already at its maximum during the first day of therapy with atenolol and no
further changes were observed during the study. Aternolol also reduced the
pressor increment during exercise. Atenolol could therefore, be said to have a
prompt and long lasting action.
ABSORPTION, METABOLISM AND EXCRETION
Atenolol is
appreciably absorbed when administered orally. It is about 20-30% bound to
plasma proteins and eliminated largely unchanged by the kidney (Rubin et al
1982). Its elimination half-life is about 7 hours.
Atenolol is
beta-1 selective and has a long half-life. Among the beta-adrenoceptor
antagonists these two properties are the ones likely to have the greatest
clinical relevance, indeed long duration of action offers the possibility of
reducing the number of daily administration of a drug and it has been shown
that the compliance of hypertensive patients to treatment is inversely
proportional to the frequency of drug administration (Finnerty et al, 1973).
TOXICITY, SIDE EFFECTS AND PRECAUTIONS
No
appreciable inhibition of bronchodilatation has been noticed with atenolol and
there is no convincing evidence that atenolol augments hypoglycaemia. However,
atenolol has to be used with caution in asthmatics and diabetics receiving
insulin or hypoglycaemic drugs.
As with all
beta-blockers atenolol should not be used if there is a risk of congestive
heart failure unless the patient is monitored closely.
THERAPEUTIC USES
The relative
selectivity of atenolol is the basis for its therapeutic advantage over less
selective agents (Ablad et al 1973). Atenolol is mainly used in the treatment
of hypertension and angina pectoris. Its selective agents (Ablad et al 1973).
Atenolol is mainly used in the treatment of hypertension and angina pectoris.
Its selective beta-1 adrenoceptors blocking activity makes it preferable to
propranolol for use in patients with mild obstructive airways disease.
1.5
PROPRANOLOL
Propranolol
was the first beta-adrenoceptor antagonist to come into wide clinical use. It
is a highly potent non-selcetive beta-adrenoceptor antagonist (blocks both
beta-1 and beta-2 adrenoceptors competitively). It does not exhibit any ISA but
has a quinidine – like action. The chemical structure is shown in fig. 1.
PHAMACOLOGICAL
PROPERTIES.
a.
Cardiovascular system: The major effect of propranolol on
the cardiovascular system is due to its actions on the heart. Propranolol
decreases heart rate and cardiac output, prolongs mechanical systole and
slightly decreases blood pressure in resting subjects (Robin et al 1967). The
effects on cardiac output and heart rate are more prominent during exercise.
Peripheral resistance is increased as a result of compensatory sympathetic
reflexes, and blood flow to all tissues except the brain is decreased (Nies et
al 1973).
Propranolol reduces sinus rate, decreases the
spontaneous rate of depolarization of ectopic pacemakers and slows conduction
in the atria and in the A.V node hence its use in the treatment of some cardiac
arrhythmias.
b. Metabolic effects: propranolol inhibits
glycogenolysis in the heart and the skeletal muscles. The effects on hepatic
glycogenolysis are dependent on species.
c.
Other effects: the most important response to beta-blockade outside
the cardiovascular system is that of the bronchi and the bronchioles.
Adrenergic bronchodilatationn is mediated by beta-2-adrenoceptors. Propranolol constantly
increases airways resistance. This effect is small and of no clinical
significance in normal individuals but is can be marked and potentially
dangerous in asthmatics (Nicholascu et al, 1972). Because bronchodilatation is
a beta-2-adrenergic response, selective beta-1-blockers, such as atenolol, are
much less likely than propranolol to induce broncho constriction and they have
been used in asthatics with minimal effects on airway resistance. (Formgren
1972).
ABSORPTION, METABOLISM AND EXCRETON
Propranolol
is almost completely absorbed following oral administration. However much of
the administered drug is metabolised by the liver during the first passage
through the portal circulation and only put to about 30% reaches the systemic
circulation. The degree of hepatic extraction of propranolol is less as the
dose is increased. Also somewhat less of the drug is removed during the first
circulation through the liver after repeated administration than after the
initial dose, which accounts for a
gradual increase in the half-life of the drug on chronic oral administration
(about 4 hours) compared with the half-life of the initial oral dose (about
3hours) (Shand 1975).
Propranolol
is about 90-95% bound to plasma proteins (Evans et al 1973). Propranolol is
virtually completely metabolised before excretion in the urine (Hayes and
Cooper 1971). One of the products of hepatic metabolism is
4-hydroxypropranolol. This metabolite is an active compound and is produced
predominantly when the drug is administered orally. Other metabolic products
that have been identified in the urine include naphthoxylactic acid,
isopropylamine and propanol glycol. A considerable fraction of propranolol is
apparently glucuronide conjugates (Shand 1975).
TOXICITY SIDE EFFECTS AND PRECAUTIONS
Abrupt
withdrawal of propranolol therapy may give rise to a withdrawal syndrome. This
may be due to the super sensitivity of beta-adrenoceptors. Some patients may
experience severe exacerbation of angina attacks may experience severe
exacerbation of angina attacks and patients being treated for hypertension may
have a life-threatening rebound of high blood pressure to levels that can
exceed pre-treatment levels. Hence withdrawal of propranolol therapy should be
gradual.
Propranolol
causes an increase in airways resistance which can be life – threatening in
asthmatics. Asthma is therefore an absolute contra indication to the use of
propranolol.
Propranolol
augments the hypoglycamic action of insulin by reducing the compensatory effect
of sympathoadrenal activation and masks the tachycardia that is an important
sign of developing hypoglycaemia. Therefore uncontrolled diabetes is an
absolute contra indication to propranolol therapy.
Other
minor side effects that have reported include nausea, vomiting, diarrhoea, and
constipation. CNS side effects include vivid dreams, night mares and
depression.
THERAPEUTIC USES
1. In the treatment of
hypertension, it is usually combined with a diuretic. It is also frequently
used as an adjunct to treatment with a vasodilator in order to minimize reflex
tachycardia.
2. It is used in the
management of both supraventricular and ventricular arrhythmia.
3. Angina pectoris
prophylaxis
4. Hypertrophic obstructive
cardiomyopathies.
5. Hyperthyroidism
(especially in thyroid crisis).
6. As a prophylaxis in
migraine therapy.
1.6
SCOPE OF THE PORJECT
Beta-adrenoceptor
antagonists are widely used in the treatment of ischaemic heart disease and
hypertension. It has been widely reported in the literature that there are
profound racial differences in the responsiveness to both selective and
non-selective beta-adrenoceptor antagonists. (Venter and Joubert 1984; salako
et al 1979; Abson et al 1981). However, the, factors underlying these
differences have not been clearly defined, beta-blockade can be assessed from
effects on:
i.
Blood pressure and heart rate’
ii.
Exercise-induced tachycardia
iii.
Lung volumes and
iv.
24 hour urinary electrolyte output (The Na+/K+
ATpase regulating potassium movement across the cell membrane is
regulated by a beta-2 – adrenoceptor (Structhers and Reid 1982).
Because there is a
scarcity of published studies in healthy blacks this study was undertaken to
assess the physiological and biochemical effects of standard doses of
oxprenolol, atenolol and propranolol. The results were later compared to
published results among age-and sex matched Caucasians with a view to
determining any differences in responsiveness. As drug levels were not measured,
their pharmacokinetics were not compared.
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