Effects Of Oxprenolol Research Articles

A preferential blocking effect of oxprenolol on alpha 1-adrenoceptors in the rat.

A preferential blocking effect of oxprenolol on alpha 1-adrenoceptors in the rat.

??-Blockade Reverses Regional Dysfunction in Ischemic Myocardium

To determine the protective effect of oxprenolol-induced beta-blockade on the compromised myocardium (critical constriction of the left anterior descending coronary artery) against the adverse effect of high concentrations of halothane, halothane dose-response curves were obtained in six dogs in each of three phases: preconstriction (control), critical constriction, and critical constriction with the addition of 0.3 mg/kg intravenous oxprenolol. The extent of depression of ventricular function was essentially the same in the three phases. However, at high halothane concentrations (2.0% inspired), the depression of systolic shortening in the compromised segment was significantly minimized after oxprenolol so that shortening was 10.2% +/- 1.8 instead of 6.5% +/- 1.4 (P less than 0.05); moreover the large increase in postsystolic shortening observed during critical constriction was abolished after oxprenolol. This suggests a protective effect of oxprenolol on regional myocardial function in the presence of critical constriction, possibly by an effect on myocardial metabolism or endocardial blood flow.

The Relative Antihypertensive Potency of Propranolol, Oxprenolol, Atenolol, and Metoprolol Given Once Daily

The antihypertensive effect of four beta-blocking agents given once daily was compared with that of placebo in a prospective, crossover, double-blind study of 150 patients. The preparations tested were slow-release propranolol hydrochloride, 160 mg, atenolol, 100 mg, slow-release oxprenolol hydrochloride, 160 mg, and metoprolol, 200 mg. Propranolol and atenolol produced a significant decline in lying, standing, and postexercise blood pressure and pulse rate values. The effects of oxprenolol and metoprolol were not significantly different from that of placebo.

The effects of oxprenolol on ambulatory intra-arterial blood pressure in essential hypertension.

Continuous intra-arterial blood pressure recording using the "Oxford" technique has been used to study the antihypertensive effects of oxprenolol taken three times daily in fully ambulatory patients with essential hypertension, outside hospital. During the first 24 h of treatment there was a reduction in daytime heart rate and a small reduction in daytime blood pressure. After 10 weeks treatment there was a more substantial fall in daytime blood pressure from the hour of waking, but no effect on sleeping nighttime blood pressure or heart rate. Twenty-four hour variation, as assessed by the amplitude of a fitted regression curve, showed a reduction in heart rate but not blood pressure variation. In 4 patients restudied after 11 weeks treatment with oxprenolol (tid) and cyclopenthiazide at 9 a.m. there was some evidence of an antihypertensive effect occurring during both the daytime and nighttime.

Effect of Oxprenolol on the Pharmacokinetics and Pharmacodynamics of Hydralazine

Hydralazine increases the bioavailability of highly lipid- soluble β- adrenoceptor antagonists, but has no significant effect on the pharmacokinetics of β- blockers such as acebutolol or nadolol. The effect of β- blockers on the pharmacokinetics of hydralazine has not previously been investigated. This study describes the reciprocal pharmacokinetic and pharmacodynamic interactions of hydralazine and slow- release oxprenolol in 6 patients with mild- to- moderate hypertension.

The acute and chronic effect of oxprenolol and propranolol on peripheral blood flow in hypertensive patients.

1 The effects of oxprenolol and propranolol on peripheral blood flow were compared in patients with mild and moderate essential hypertension. 2 In an acute double-blind crossover study in which eight patients participated there was a significant reduction in resting forearm blood flow (RFBF) 2 h after 80 mg propranolol (mean +/- s.e. mean) (-0.87 +/- 0.13 microliter min-1 100 g-1) and after 80 mg oxprenolol (-0.30 +/- 0.12) but not after placebo. This reduction was significantly greater after propranolol (P = 0.022). 3 Seven patients continued into a double-blind crossover study comparing the above dose of the two drugs twice a day. On both the beta-adrenoceptor blockers there was a significant reduction in blood pressure after 2 weeks of treatment and also a significant reduction in RFBF. 4 After 6 weeks treatment with propranolol the reduction in RFBF persisted and was significantly less (P = 0.04) than after 6 weeks treatment of oxprenolol, at which time RFBF was back to control. 5 There were no consistent changes in skin temperature. 6 Neither propranolol nor oxprenolol should be used in patients with severe peripheral vascular disease. 7 If beta-adrenoceptor blockade is necessary in patients with mild peripheral vascular disease oxprenolol should be used in preference to propranolol but should be prescribed with caution.

Effect on High Density Lipoprotein Cholesterol of Atenolol and Oxprenolol in Patients with Mild Essential Hypertension

1. Nineteen healthy men aged 50 years, with untreated, mild essential hypertension WHO group I, were randomized into two groups to study the effect of treatment (18 weeks) with oxprenolol (n = 10) and atenolol (n = 9) on serum cholesterol fractions, total triglycerides and uric acid. 2. Oxprenolol lowered high density lipoprotein (HDL) cholesterol by 11.4% (P < 0.02) and cholesterol ratio (HDL cholesterol × 100/LDL + VLDL cholesterol) by 13.7% (P < 0.05). Atenolol lowered HDL cholesterol by 16.5% (P < 0.02) and cholesterol ratio by 19.2% (P < 0.01). 3. Oxprenolol and atenolol raised total triglycerides by 20.0% and 17.9% respectively. Only with atenolol was this increment statistically significant (P < 0.05). 4. The HDL cholesterol lowering effect of oxprenolol and atenolol observed in the present study may have clinical importance, since such metabolic side effects have been postulated to counteract the beneficial effect of blood pressure reduction on development of atherosclerosis and coronary heart disease in mild essential hypertension.

Effects of oxprenolol on the intra-arterial blood pressure response to dynamic exercise in hypertensive men.

The intra-arterial blood pressure of 20 male patients with essential hypertension was continuously recorded during dynamic exercise. Graded exercise testing on a bicycle ergometer and a stair-climbing test were performed prior to and during treatment with oxprenolol. Acute oxprenolol therapy was associated with a reduction in heart rate but little reduction in blood pressure. Chronic treatment for 14.3 weeks with oxprenolol (mean daily dose, 344 mg) was associated with a substantial reduction of blood pressure at rest and at each level of bicycle exercise. A similar antihypertensive effect was demonstrated during stair climbing. The normal blood pressure response to exercise as assessed by the relative (percentage) increase in pressure above the pre-exercise level and the rate of increase in blood pressure (per unit of work), as well as exercise tolerance, were unchanged by chronic beta-blockade with oxprenolol.

Beta blockade and diabetes mellitus: Effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in insulin-dependent diabetics

The effect of the administration of a single oral dose of placebo, oxprenolol, and metoprolol on insulin-induced hypoglycemia was investigated in seven insulin-dependent diabetics in a double-blind randomized study. Neither of the β-blocking agents accelerated the plasma glucose lowering effect of insulin. Plasma glucose recovery from hypoglycemia was grossly impaired in diabetics whether blocked or not, and all investigations had to be terminated by i.v. glucose injection after 1 hr of sustained hypoglycemia. During the period of observation, no further delaying effect by either β-blocker was observed. The lack of plasma glucose recovery seems to be at least in part related to a retarded and reduced glucagon response to hypoglycemia. Both drugs blocked the hypoglycemia-induced pulse rate increase, but neither caused bradycardia. A significant increase in diastolic pressure was recorded with oxprenolol, whereas a drop in systolic pressure was noted with metoprolol. Oxprenolol suppressed the NEFA rise after insulin-infusion termination to a greater extent than did metoprolol. Hypoglycemic symptoms were not affected by β-blockade. The results suggest that neither drug further worsens the already grossly impaired plasma glucose recovery, but that oxprenolol and metoprolol may differ in their effects on hemodynamic response to hypoglycemia. This aspect of the problem requires further study under careful control in hypertensive diabetics.

Beta blockade and diabetes mellitus: Effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in normal subjects

In a double-blind randomized study, the effect of the acute administration of a single oral dose of oxprenolol, a nonselective β-blocker, and of metoprolol, a β 1 selective blocker, on insulin-induced hypoglycemia was tested in seven normal subjects. Neither of the drugs potentiated the hypoglycemic effect of insulin. The recovery from hypoglycemia was delayed by both blocking agents only in the late phases of the experimental observation. This effect could not be accounted for by suppression of release of the counterregulatory hormones glucagon or cortisol, but may be mediated by the inhibition of NEFA and gluconeogenic-substrate release in response to hypoglycemia. Both drugs blocked the hypoglycemia-induced tachycardia. Only oxprenolol raised diastolic blood pressure during hypoglycemia. Symptoms of hypoglycemia were not masked by either blocking agent, and sweating was enhanced and prolonged by both drugs. Thus, no clear-cut differences in the glycemic response to insulin-induced hypoglycemia were found between metoprolol and oxprenolol, but the drugs differed in their influence upon the blood pressure response to insulin-induced hypoglycemia.

β-Adrenoreceptor Blockade and Diabetes Mellitus: Effect of Oxprenolol and Metoprolol on the Metabolic, Cardiovascular and Hormonal Response to Insulin-Induced Hypoglycaemia in Insulin-Dependent Diabetic Patients

β-Adrenoreceptor Blockade and Diabetes Mellitus: Effect of Oxprenolol and Metoprolol on the Metabolic, Cardiovascular and Hormonal Response to Insulin-Induced Hypoglycaemia in Insulin-Dependent Diabetic Patients

β-Adrenoreceptor Blockade and Diabetes Mellitus: Effect of Oxprenolol and Metoprolol on the Metabolic, Cardiovascular and Hormonal Response to Insulin-Induced Hypoglycaemia in Normal Subjects

<i>β</i>-Adrenoreceptor Blockade and Diabetes Mellitus: Effect of Oxprenolol and Metoprolol on the Metabolic, Cardiovascular and Hormonal Response to Insulin-Induced Hypoglycaemia in Normal Subjects

Adrenaline activation of prejunctional beta-adrenoceptors in guinea-pig atria.

1. Adrenaline in a concentration of 1.0 microM depressed the stimulation-induced efflux of tritium from the guinea-pig atria incubated with [3H]-noradrenaline, whereas adrenaline in a concentration of 0.5 nM significantly enhanced the stimulation-induced efflux of tritium. This enhancement was blocked by metoprolol (0.1 microM) and thus appears to be mediated by beta-adrenoceptors. 2. In guinea-pig atria incubated with unlabelled adrenaline and then with [3H]-noradrenaline, both catecholamines were released by field stimulation. In such atria metoprolol, practolol, oxprenolol or propranolol decreased the stimulation-induced efflux of tritium. These effects did not occur if the atria were incubated with unlabelled noradrenaline and then with [3H]-noradrenaline, suggesting that neuronally released adrenaline activates prejunctional beta-adrenoceptors. 3. The effect of oxprenolol in decreasing the release of tritium from guinea-pig atria, incubated with unlabelled adrenaline and then with [3H]-noradrenaline was greater in the presence of phentolamine. This may reflect the alpha-adrenoceptor blocking activity of oxprenolol.

Effects of oxprenolol and propranolol on systolic time intervals

Twenty patients with coronary heart disease participated in a double-blind, randomized, crossover study on three study mornings to evaluate the effect of oral oxprenolol 80 mg, oral propranolol 80 mg, and placebo on left ventricular contractility. Systolic time intervals were performed in the control period and at 60, 90, 120, 150, 180, 240, 300, and 360 min after medication. None of 20 patients developed adverse effects. The 80-mg doses of oxprenolol and propranolol had a negative chronotropic effect, with the resting heart rate slightly but consistently decreased more after propranolol, attaining statistical significance at 90, 150, and 300 min. That the 80-mg doses of oral oxprenolol and propranolol also induced a negative inotropic effect was indicated by a similar prolongation of the external isovolumic contraction time and pre-ejection period intervals. This equipotent dose of oxprenolol in producing a negative inotropic effect induces less resting bradycardia than propranolol.

Smoking and catecholamine and c-AMP concentrations in the coronary circulation of man and the effect of oxprenolol

Changes in catecholamine, c-AMP and lactate concentrations in the coronary circulation of man, during smoking, were studied in 12 patients. The heart rate increase from 63 +/- 2 beats/min (control) to 74 +/- 3 (smoking)(P less than 0.01), falling to 70 +/- 2 (10 min after smoking) (0.05 greater than P greater than 0.01), whilst coronary sinus c-AMP concentrations rose from 11 +/- 0.7 nmol/l (smoking) to 11.9 +/- 0.8 nmol/l (after smoking) (0.05 greater than P greater than 0.01; one tailed 't' test). There was no significant change in blood pressure, catecholamine or lactate concentrations. The study was repeated in eight of the patients following intravenous oxprenolol. Coronary sinus catecholamine concentrations increased from 4.1 +/- 0.7 nmol/l (control) to 5.5 +/- 1.1 nmol/l (after smoking) (0.05 greater than P greater than 0.01; one tailed 't' test), but heart rate and c-AMP concentrations remained unchanged, confirming that smoking-induced tachycardia is a result of a beta-adrenergic mechanism, at least part of which is due to a release of cardiac catecholamines. Arterial lactate concentrations increased only following oxprenolol from 0.74 +/- 0.07 mmol/l (control) to 0.83 +/- 0.09 mmol/l (smoking).

Effect of oxprenolol on some fear-induced behavioral responses and hyperthermia in rats subjected to inescapable shocks.

The effect of oxprenolol (100 mg/kg p.o.) on the development of hyperthermia in a shock enclosure and on exploratory and grooming responses in an exploration box, was investigated in rats subjected to inescapable shocks once daily for 5 days. The hyperthermic response of shocked rats was found to be significantly reduced by oxprenolol treatment. Exploratory behavior, which was suppressed by previous exposure to shocks, was not influenced by oxprenolol. However, under oxprenolol treatment grooming diminished from the first day of the trial onward, both in duration and frequency, as though habituation had occurred. The results are interpreted as evidence of partial effectiveness of oxprenolol in suppressing fear-induced somatic and behavioral manifestations.

Comparison of the beta adrenergic blocking properties and negative inotropic effects of oxprenolol and propranolol in patients

Comparison of the beta adrenergic blocking properties and negative inotropic effects of oxprenolol and propranolol in patients

HEMODYNAMIC EFFECTS OF OXPRENOLOL ALONE AND COMBINED WITH NITROGLYCERIN IN PATIENTS WITH ISCHEMIC HEART DISEASE

Abstract In 16 males with ischemic heart disease the acute hemodynamic effects of a new β‐blocker, oxprenolol, have been studied during rest and exercise by right heart catheterization technique. The myocardial oxygen‐saving effect of oxprenolol was demonstrated by a significant reduction of heart rate during exercise and a widened arterio‐venous oxygen difference. Addition of nitroglycerin rapidly and markedly reduced myocardial oxygen demand by reducing the left ventricular filling pressure and the mean systemic arterial pressure. Oxprenolol and nitroglycerin can be combined without any untoward effects and without loss of efficiency of either drug. However, no evidence of synergism between the two drugs was found in this study.

The effects of oxprenolol (Trasicor, Ciba 39089-Ba) on patterns of urinary sodium excretion in man

The effects of oxprenolol (Trasicor, Ciba 39089-Ba) on patterns of sodium excretion were evaluated in normal subjects and in patients with cardiac disease. In normal subjects 120 mg of oxprenolol daily caused a slight but significant increase in sodium excretion, and the day/night sodium excretion ratio was reversed in 60 percent. With doses of 240 mg, the sodium excretion in these subjects fell to control levels, but the excretion ratio was reversed in all. In patients with cardiac disease with incipient failure sodium was not retained during treatment with either 120 mg or 240 mg of oxprenolol daily. In 1 patient with ischemic heart disease receiving 120 mg of propranolol daily sodium was retained and frank heart failure was precipitated whereas 240 mg of oxprenolol produced no change. Differences between oxprenolol and propranolol in antagonizing beta receptor excitation and depressing myocardial contractility are discussed. The direct negative inotropic action of this group of drugs may also contribute to the changes in patterns of sodium excretion induced by beta receptor blockade.

EFFECT OF OXPRENOLOL ON ADRENALINE-EVOKED VENTRICULAR ARRHYTHMIAS IN DOGS ANAESTHETIZED WITH HALOTHANE IN OXYGEN

SUMMARY The effect of oxprenolol (CIBA 39,089-Ba), a recently introduced adrenergic beta-receptor antagonist, on adrenaline-evoked ventricular arrhythmias was studied in atropinized dogs anaesthetized with halothane in oxygen. The anti-arrhythmic activity of oxprenolol was due to specific blockade of beta-receptors. The block produced was surmountable in nature and larger doses of adrenaline re-evoked ventricular arrhythmias. Its potency was very similar to that of propranolol. However, in contrast to propranolol, oxprenolol administration following electrical defibrillation of the heart did not precipitate cardiocirculatory collapse. In this respect oxprenolol may have important therapeutic advantages over propranolol.