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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:

  • INTRODUCTION AND LITERATURE REVIEW
  • MECHANISM OF ACTION OF BETA-ADRENOCEPTOR BLOCKERS
  • OXPRENOLOL
  • ATENOLOL
  • PROPRANOLOL
  • 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:

  1. Blood pressure and heart rate
  2. Exercise-induced tachycardia
  3. Lung volumes
  4. 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

  • 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.

  • 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.

  1. 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.

  1. 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.

  1. 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.

  • 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.

 

  • 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.

  • 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.

  1. 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.

  1. Metabolic effects: propranolol inhibits glycogenolysis in the heart and the skeletal muscles. The effects on hepatic glycogenolysis are dependent on species.
  2. 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.
    • 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:

  1. Blood pressure and heart rate’
  2. Exercise-induced tachycardia
  • Lung volumes and
  1. 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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