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PubMed1977

An investigation of "absolute plasma level effect relationships" and "absolute cardioselectivity" with respect to beta-adrenoceptor blockade.

In a group of 6 healthy (but physically unfit) volunteers an investigation was made of whether there was a true plasma level effect relationship and absolute "cardioselectivity" with respect to beta-adrenoceptor blockade due to practolol. To this end three treatments were given orally, namely placebo, practolol 100 mg and practolol 400 mg. Cardiac beta-adrenoceptor blockade was assessed by measuring the inhibition of exercise heart rate and pulmonary beta-adrenoceptor blockade was assessed by measuring the reduction in exercise peak flow rate, up to 24 h after each dose. Plasma practolol levels were determined spectrophotometrically. From the results obtained there was no reason to doubt the existence of a valid relationship between cardiac beta-adrenoceptor blocking activity and the plasma concentration of practolol. It was also concluded that even in non-asthmatics, practolol does not possess absolute "cardioselectivity" since significant reductions in peak flow rate were discernible during vigorous exercise, particularly when the large dose had been given.

Adult↗
PubMed1976

The nature of the beta-adrenoreceptor controlling plasma renin activity in man.

1. Seven healthy sodium-replete male volunteer subjects remained supine during and for at least 1 h before the study. Heart rate and blood pressure were recorded continuously, and peripheral venous blood samples were taken every 15 min for determinations of plasma renin activity. 2. All subjects were studied twice: after 3 days of oral practolol (100 mg, three times daily) and after a similar period on placebo. Each study consisted of an intravenous infusion of isoprenaline in graded doses (0-20 microng/min in the placebo phase; 0-16 microng/min in the practolol phase), followed after rest for 2 h by an intravenous infusion of salbutamol (0-20 microng/min after placebo; 0-80 microng/min after practolol). 3. Both salbutamol and isoprenaline produced dose-related increases in systolic blood pressure, heart rate and plasma renin activity and decreases in diastolic pressure. 4. The increases in heart rate and plasma renin activity induced by either agonist were competitively blocked by practolol, as was the fall in diastolic blood pressure induced by isoprenaline; the salbutamol-induced fall of diastolic blood pressure was unaffected by practolol. 5. Comparison of dose ratio--1 estimates confirmed that practolol selectively blocked increases in heart rate and plasma renin activity due to salbutamol; no selective blockade against isoprenaline-induced changes was shown. 6. Selective blockade of salbutamol-induced changes indicate that a beta1-adrenoreceptor mediates changes in plasma renin activity.

Albuterol↗
PubMed1976

Effect of cardioselective beta-blockade on heart function and chest pain in acute myocardial infarction.

Systolic time intervals and the a/H ratio were recorded in 20 patients with uncomplicated acute myocardial infarction over a period of five days. The initial high heart rate and systolic blood pressure and the short PEP and ICT indicating a sympathetic overactivity were spontaneously normalized during the first week of infarction. LVET was reduced indicating a fall in stroke volume and the a/H ratio was unchanged at the high levels suggestive of elevated preload or LVEDP. In 10 patients with acute myocardial infarction and recurrent chest pain recordings on noninvasive parameters were made before and 30 min after intravenous injection of practolol. In addition, 7 patients with chest pain, classified as acute myocardial infarction, were given practolol. The average dose of practolol was 17.9 mg ranging from 5 to 30 mg. An almost immediate and pronounced relief of pain was observed in all patients and no signs of impaired left ventricular function appeared. The product of systolic blood pressure and heart rate was decreased by practolol and the PEP and the ICT were prolonged to normal values while no changes were seen in LVET and a/H ratio. On 126 occasions practolol was given in dosages ranging from 5 to 30 mg (mean 8 mg) to 75 patients with acute myocardial infarction and recurrent chest pain. A satisfactory pain relief was seen on 108 occasions. It is suggested that an inappropriate sympathetic overactivity is an important factor in provoking recurrent chest pain in acute myocardial infarction. Administration of the beta-adrenergic blocking agent practolol resulted in pain relief due to reduction of heart work and in severity of myocardial ischemia. The beta-blocking agent was well tolerated in the present study. Continuous beta-blockade during the whole hospital stay to patients with acute myocardial infarction seems to be a very attractive therapy in order to preserve the ischemic myocardium and limit the size of infarction.

Acute Disease↗
PubMed1971

Responses of coronary vessels to adrenergic stimuli.

Coronary responses to adrenergic stimuli were determined in the intact beating heart before and after administration of practolol, 4-(2-hydroxy-3-isopropylaminoproproxy) acetanilide, which in low doses blocks myocardial but not vascular beta receptors. The left circumflex coronary artery of dogs was perfused with arterial blood at constant flow, and coronary perfusion pressure was measured. Before practolol, intracoronary injections of isoproterenol and norepinephrine and electrical stimulation of left cardiac sympathetic nerves caused reductions in perfusion pressure or vasodilatation associated with increases in left ventricular dp/dt, heart rate, and systolic pressure. After practolol, the coronary vasodilator response to isoproterenol was reduced by about 30% and occurred without significant changes in dp/dt, heart rate, and pressures. The addition of propranolol blocked completely the coronary responses to isoproterenol. Vascular responses to isoproterenol in the paw were not altered by practolol. Practolol antagonized the increases in dp/dt, heart rate, and systolic pressure and reversed coronary responses to norepinephrine and nerve stimulation from dilatation to constriction. The constriction, in turn, was reduced or reversed by phentolamine, an alpha receptor antagonist. Propranolol did not augment the constriction seen in response to norepinephrine and nerve stimulation after practolol. These results indicate that the coronary vasodilator action of norepinephrine and sympathetic nerve stimulation is indirect and caused by stimulation of myocardial beta receptors. The direct effect of these two stimuli on coronary vessels is minimal and is mediated through stimulation of alpha (vasoconstrictor) receptors. In contrast, the coronary vasodilator response to isoproterenol is both direct and indirect, resulting from stimulation of vascular and myocardial beta receptors; the direct vascular effect predominated in this study.

Adrenergic beta-Antagonists↗
PubMed1976

[Cyclic AMP and plasma renin activity in renal vein blood after amitryptiline, theophylline, furosemide and beta adrenergic blocking substances (author's transl)].

The influence of amitryptiline, theophylline and furosemide on the concentration of cyclic-AMP and plasma renin activity (PRA) was investigated in renal vein plasma. Additionally, the stimulating effect of furosemide on the PRA after application of the beta-adrenergic receptor antagonists propranolol and practolol and the cyclic AMP concentration in the plasma were measured. All drugs were given intravenously. After amitryptiline cyclic-AMP concentration increased about 1.5-fold compared with the basal value,PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold compared with the basal value, PRA was not altered. After theophylline cyclic-AMP concentration increased about 1.2-fold, PRA 2.0-fold coa increased within 7 min and no further increase was observed till the 15th min. After practolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value within 10 min. The stimulating effect of subsequently applied furosemide on PRA was not altered, but the cyclic-AMP concentration was not changed in this time by furosemide. After propranolol cyclic-AMP concentration and PRA decreased about 20% compared with the basal value. The cyclic-AMP concentration was not influenced by the following furosemide application, in agreement with the findings after practolol, however, PRA could be stimulated only in 36% of these patients under beta-receptor blockade. Our results show that changes of the concentrations of cyclic-AMP and of PRA are independent of each other. An elevated intracellular cyclic-AMP level due to the inhibition of phosphodiesterase is as a single factor unable to stimulate renin release. Our results give no evidence of a direct involvement of the adenylcyclase-system in the mechanism of renin release. The effect of propranolol and practolol on the basal value of PRA and cyclic-AMP is equal. The different influence of 10 mg propranolol and 20 mg practolol on the stimulating effect of 40 mg furosemide on the PRA can be interpreted as a dosage problem.

Adrenergic beta-Antagonists↗
PubMed1980

The effect of a selective beta adrenergic blocking agent on ventricular arrhythmias in the first year following myocardial infarction.

Fifty-five patients with recent acute myocardial infarction entered a single-blind cross-over trial to assess the effect of oral practolol 200 mg twice daily on the incidence and nature of ventricular arrhythmias in the first year following myocardial infarction. Patients had 24-hour Holter electrocardiogram tape monitoring at two weeks following infarction and at three-monthly intervals for one year. Twenty-six patients completed the full year of the trial with 12% of tape recordings technically unsatisfactory. A total of 46 periods of comparison of the action of practolol versus placebo therapy were available in thirty patients. Whilst receiving the selective beta adrenergic blocking agent, practolol, there was a significant reduction in the percentage of studied hours during which salvos of ventricular premature beats occurred (P < 0.025), however the percentage of patients in whom salvos were recorded was unchanged. The incidence of all other ventricular arrhythmias was not reduced in the practolol group. When the effect of practolol was related to the site of infarction, anterior or inferior, there was no significant reduction in the incidence of ventricular arrhythmias.

Adult↗
PubMed1974

The effects of three beta-adrenoceptor blocking drugs on isolated preparations of skeletal and cardiac muscle.

1 The effects of propranolol, oxprenolol and practolol on the isometric twitch responses to electrical stimulation of isolated diaphragm muscles from the rat and of isolated papillary muscles from the rabbit are described.2 Depression of the twitch responses of the diaphragm muscle was produced by propranolol (20 mug/ml), by oxprenolol (100 mug/ml) and by practolol (500 mug/ml).3 Depression of the twitch responses of the papillary muscles was produced by propranolol (20 mug/ml) by oxprenolol (100 mug/ml) and by practolol (200 mug/ml).4 No increase of twitch tension was produced by oxprenolol or practolol on either tissue.5 It is concluded that propranolol, oxprenolol and practolol produce negative inotropic actions on isolated cardiac muscle by a mechanism unrelated to blockade of beta-adrenoceptors and which occurs at doses which are well in excess of those doses required to produce beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1980

Effects of beta-adrenergic blocking drugs in hypertensive rats.

Antihypertensive effects of three beta-adrenergic blocking drugs, acebutolol, propranolol, and practolol were studied for 11 weeks. Spontaneously (SHR); one-clip, two-kidney (CLIP); and deoxycorticosterone and salt (DOC) hypertensive rats were used. The drugs were given orally, 100 mg/kg per day, 5 days per week before development of hypertension. Propranolol inhibited blood pressure (BP) increase significantly in SHR. Acebutolol and practolol also lowered BP in SHR. Three drugs did not affect BP in CLIP, but an apparent inhibition was seen when the results were analyzed including the cases of which BP stayed below 150 mmHg. Either of three drugs did not show antihypertensive effects in DOC. Acebutolol rather increased BP more rapidly. Practolol also increased BP slightly more rapidly. Cerebral stroke was seen in DOC. The incidences of the stroke in the groups given the solvent, acebutolol, propranolol, and practolol were 3/6, 4/7, 2/6, and 3/6, respectively. Acebutolol seemed to cause stroke earlier with the more rapid BP elevation. Acebutolol, propranolol, and practolol decreased incidence of the vascular disease in CLIP. Propranolol also decreased it in DOC. Plasma renin activity was suppressed by these drugs in SHR and CLIP. The mechanisms of antihypertensive effects of beta-adrenergic blocking drugs are unknown. The present study denies those due to inhibition of cardiac function, or renin release from the kidney. A better experimental model is necessary to study this. The possibility that acebutolol and other beta-blockers might accelerate BP elevation and incidence of stroke must be reexamined.

Acebutolol↗
PubMed1975

Role of adrenergic mechanisms in the development of cardiac hypertrophy.

This experiment was designed to study the role of cardiac beta-adrenergic mechanisms in the development of hypertrophy in rats. The suprarenal abdominal aorta was banded, resulting in an increase in cardiac wt-body wt ratio. A group of rats received a sham operation. Half of the banded rats were treated with practolol, 2.0 mg/kg intraperitoneally every 12 hr for the 6 days after banding. The effectiveness of cardiac beta-adrenergic blockade was confirmed by absence of an increase in heart rate following intravenous isoproterenol at various times between practolol injections. Practolol did not affect the gradient in the banded groups. Six animals in each banded group were sacrificed daily for 6 days. The right and left ventricles were dissected separately and weighed. RV-body weight ratios increased similarly in both banded groups. LV-body weight ratio (g/kg) was 2.17 +/- 0.043 in sham rats, and it attained maximal levels of 3.03 +/- 0.10 within 6 days in banded untreated rats and 2.96 +/- 0.14 in banded rats receiving practolol. Therefore, beta-adrenergic mechanisms were not involved in the development of hypertrophy due to increased afterload. Also, these findings are not consistent with the Meerson hypothesis, since hypertrophy occurred despite the reduction in myocardial O2 consumption due to practolol.

Animals↗
PubMed1979

Hypotensive action of OPC-1427, a new beta-adrenergic blocking agent in rats.

8-Acetonyloxy-5-[3-(2-(3,4-dimethoxyphenyl)-ethylamino)-2-hydroxypropoxyl]-3,4-dihydrocarbostyril (OPC-1427), is a newly synthesized cardioselective beta-adrenoceptor blocking agent and we examined the effects of this compound given intraperitoneally to consious Kyoto Wistar normotensive (WKR), spontaneous hypertensive (SHR) and DOCA-NCl hypertensive (DOCA rat) rats. The results were compared to findings with propranolol and practolol. OPC-1427 produced a significant hypotensive action in SHR and DOCA rats and this effect was less in WKR. With propranolol and practolol effective hypotensive effects were seen in WKR and DOCA rats but not in the SHR. The efficacy of the hypotensive action of these agents was propranolol greater than OPC-1427 = practolol in WKR, OPC-1427 greater than practolol in SHR, and OPC-1427 greater than practolol = propranolol in DOCA rats. Thus OPC-1427 appears to be a promising beta-adrenoceptor blocking agent which exerts a hypotensive state, as demonstrated in hypertensive rats.

Adrenergic beta-Antagonists↗
PubMed1979

[Effect of acebutolol, a cardioselective beta-adrenoceptor blocking agent, on the blood pressure in rats (author's transl)].

The effects of acebutolol, a cardioselective beta-adrenoceptor blocking agent, on the systolic blood pressure and heart rate were investigated in conscious Kyoto Wistar normotensive rats (WKY), spontaneously hypertensive rats (SHR) and DOCA-NaCl hypertensive rats (DOCA rats) and the results compared with those of propranolol and practolol. In WKY and DOCA rats, the intraperitoneal administration of acebutolol, propranolol and practolol (0.5 approximately 20 mg/kg) produced a hypotensive action, however, these effects were observed only with restricted doses and there was no evidence of a dose-dependency. The heart rate was decreased by acebutolol and propranolol, but was increased by practolol which possesses an intrinsic sympathomimetic activity. In SHR, propranolol produced a dual action, a slight rise followed by a slight fall, the change not being significant, while practolol induced a slight hypertension. On the other hand, acebutolol in high doses induced a dose-dependent hypotensive action. The heart rate was markedly and dose-dependently decreased by these three agents. Thus, while propranolol and practolol produced hypotensive effects in WKY and DOCA rats, acebutolol produced hypotensive effects in WKY, SHR and DOCA rats. These results suggest that acebutolol is a beta-adrenoceptor blocking agent which possesses hypotensive activity in hypertensive rats.

Acebutolol↗
PubMed1981

[Hemodynamic effects of some beta-adrenergic blocking agents in conscious spontaneously hypertensive rats (author's transl)].

The hemodynamic effects of propranolol, pindolol and practolol were investigated i conscious spontaneously hypertensive rats (SHR). Mean blood pressure (MBP), heart rate (HR) ard cardiac output (CO) were measured and total peripheral resistance (TPR) was calculated. CO was determined by the modified dye dilution method using an arterio-venous shunt between the left carotid artery and the right jugular vein. Intraperitoneal administration of propranolol (5 mg/kg), pindolol (0.1 mg/kg) or practolol (50 mg/kg) caused a sustained antihypertensive effect of a similar degree. The antihypertensive effect of propranolol (20-30 mmHg, 0.5-8 hr) was attributed to an early decrease of CO (0.5-4 hr) followed by a reduction of TPR (6-8 hr), while that of pindolol or practolol (30-50 mmHg, 0.5-8 hr, 30 mmHg, 2-8 hr) was apparently related to a reduction of TPR with a CO increment. HR decreased with propranolol but increased with pindolol, while only slight changes were observed with practolol. Antihypertensive effects of propranolol, pindolol or practolol were associated with characteristic hemodynamic changes.

Adrenergic beta-Antagonists↗
PubMed1976

Cutaneous reactions to propranolol (Inderal).

Six patients wit psoriasiform cutaneous eruptions that developed during long-term therapy with propranolol (Inderal) have been studied. The cutaneous changes closely resembled those seen during treatment with practolol (Eraldin). The duration of treatment before the rash was recognized averaged 10 months, which is about the same latency period as in patients with practolol-induced exanthemas. The exanthemas disappeared gradually within 1-5 weeks after treatment with propranolol had been stopped. In 4 of 5 patients the skin eruptions reappeared within 2-4 days after oral challenge with propranolol. In the fifth patient, who developed a rash after challenge with practolol and severe abdominal colics after challenge with oxprenolol, no further provocation tests with propranolol were attempted. Skin biopsies obtained from 3 patients showed a microscopical picture similar to that seen in practolol exanthemas. The pathogenetic mechanism responsible for these adverse cutaneous reactions is unknown. However, since the possibility exists, that these changes may be caused by blockade of the epidermal beta-receptors, it is recommended that all patients receiving beta-blocking drugs should be examined carefully for similar adverse reactions. Special attention should be drawn to the reversible skin changes, since during treatment with practolol these have often preceded serious complications from other organs.

Aged↗
PubMedDate not supplied

Beta-adrenoreceptor antagonists enhance the benzodiazepine-induced suppression of footshock induced fighting in mice.

Aggressive behavior in the footshock induced fighting test (FIFT) was studied after treatment with benzodiazepines (diazepam, nitrazepam, temazepam, medazepam) given alone or in combination with beta-adrenoreceptor antagonists (propranolol, oxprenolol, practolol). With the combinations of those drugs it was found that diazepam (0.5 mg/kg) with propranolol, oxprenolol, and practolol (20 mg/kg); nitrazepam (0.25 mg/kg) with propranolol (10 mg/kg) and nitrazepam (0.1 mg/kg) with practolol (20 mg/kg); temazepam (0.5 mg/kg) with propranolol (10 mg/kg) and temazepam (1 mg/kg) with oxprenolol and practolol (20 mg/kg); medazepam (1.5 mg/kg) with propranolol (10.mg/kg) and medazepam (1 mg/kg) with practolol (20 mg/kg) produced a statistically significant decrease in frequency of fighting episodes in mice as compared with benzodiazepines alone and with control animals. The results demonstrate that beta-adrenoreceptor antagonists potentiate the antiaggressive action of benzodiazepines when given in doses which by themselves do not suppress aggression.

Adrenergic beta-Antagonists↗
PubMed1977

Presence of beta-adrenoreceptors in the hypothalamus; their importance for the pressor response to hypothalamic stimulation.

The posterior hypothalamus of cats anaesthetized with pentobarbital sodium was superfused and electrically stimulated with a push-pull cannula. Superfusion of the hypothalamus with (+/-)-, (-)-propranolol, sotalol, practolol or metoprolol caused a concentration-dependent inhibiton of the pressor response to hypothalamic stimulation. (+/-)-Propranolol and a procaine concentration equi-anaesthetic to the concentration of (+/-)- and (-)-propranolol were ineffective. Lower concentrations of propranolol and metoprolol were needed to inhibit the pressor response than of sotalol or practolol. Superfusion with practolol and tolazoline impaired the pressor response to a greater extent than did superfusion with each of the drugs alone. Hypothalamic superfusion with isoproterenol elicited a concentration-dependent enhancement of the rise of blood pressure during electrical stimulation of the hypothalamus. It is concluded that beta-adrenorecptors are present in the posterior hypothalamus and that they are involved in the pressor response elicited by electrical stimulation of the hypothalamus. Propranolol and metoprolol seemed to possess a higher affinity to the beta-receptors of the hypothalamus than sotalol or practolol.

Animals↗
PubMed1976

Beta-adrenergic receptor blocking drugs in spontaneous hypertension.

Eleven beta-adrenergic receptor blocking agents and derivatives were evaluated for their ability to affect systolic arterial blood pressure and pulse rate in unanesthetized, male spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto (WKY) controls. Animals ranged from 7 to 76 weeks of age. The subcutaneous injection of 5 and 45 mg/kg metoprolol in 52 to 64 week old SHRs and 45 mg/kg twice a day to 26 to 29 week old SHRs produced a significant decrease in blooc pressure. The subcutaneous injection of pindolol (0.1 and 1.0 mg/kg) produced a greater and more consistent depressor effect in mature SHRs. The subcutaneous administration of sotalol (100 mg/kg) and alprenolol (20 mg/kg) resulted in a depressor action which was significant 120 minutes after injection of the drug. In the doses used, propranolol, oxprenolol, 4-hydroxypropranolol and K9-1366 produced pressor effect in SHRs. Propranolol did not cause this pressor effect in prehypertensive (seven week old) SHRs. Practolol, dextro-propranolol and KO-1313 had no effect on blood pressure in the doses used. Propranolol, pindolol, metoprolol, dextro-propranolol, 4-hydroxypropranolol, practolol, oxprenolol, KO-1366 and KO-1313 produced no significant effects on blood pressure in normotensive WKY controls in the doses tested. Placing oral doses of 160 mg/kg/day of metoprolol in the drinking water for seven days significantly lowered blood pressure in 14 week old SHRs previously exposed to ineffective doses of 77 mg/kg/day for 24 days. The administration of oral doses of oxprenolol (40 mg/kg/day) in drinking water for three weeks had a slight but insignificant pressor effect. Smaller doses of metoprolol (15 and 39 mg/kg/day for three to four weeks) and practolol (70 to 85 mg/kg/day for two weeks) had no effect on 52 week old SHRs. Oral doses of pindolol, metoprolol, practolol and oxprenolol had no significant effect on blood pressure in WKY controls. There was no clear relationship between the effects of the drugs on blood pressure and their ability to affect the pulse rate. Similarly, there did not appear to be any consistent relationship between the potency of the beta-blocking drug and the blood pressure lowering action. In addition, neither cardioselective beta-blockade nor sympathomimetic properties allowed the prediction of blood pressure responses to the administration of those agents possessing these features. Although SHRs provide a valuable model of human essential hypertension, the variable effects reported here and elsewhere in the literature require caution as to the applicability and usefulness of testing and evaluating beta-adrenergic blocking drugs for theri potential anti-hypertensive effects in this particular form of experimental hypertension.

Adrenergic beta-Antagonists↗
PubMed1975

[Clinical studies on the effect of drugs used in the treatment of angina].

The report is based on a four-centre study on 25 patients with coronary insufficiency (ECG signs). In random sequence the following were given to each patient: a nitrate (isosorbide dinitrate), carbocromene, practolol, and oxyphedrine. The initial criterion for inclusion was S-T depression of 0.2 mV on stepwise exercise (bicycle ergometry). S-T depression, systolic blood pressure and heart rate changes were used as criteria. For each drug there was an acute test and a long-term test of 12 days. The Friedman test was used for the statistical evaluation of the results. Isosorbide dinitrate decreased the extent of S-T depression in the acute tests while practolol did so in the long-term test. Practolol reduced systolic pressure on long-term administration, with no difference in the acute experiment. Heart rate was reduced by practolol both acutely and long-term. These results give no indication for any possible differential treatment of coronary insufficiency, but this may be due to the selection of patients in this study.

Adult↗
PubMed1975

The effects of prolonged beta-adrenoceptor blockade on heart weight and cardiac intracellular potentials in rabbits.

Estimates were made in vivo in rabbits of the relative beta-receptor blocking potency and duration of action of propranolol and practolol. In further experiments groups of litter mates were injected twice daily with approximately equi-active amounts of propranolol or practolol, or with saline, for several weeks. The heart weights of the treated animals were significantly lower than those of the controls, the water contents were higher, and the dry weight differences were highly significant; -16.8% after 2 mg/kg bd propranolol for six weeks and -33.8% after 10 mg/kg practolol. (The treated animals grew less rapidly than the controls; when corrected for body weight these figures were -11.9% and -20.4%, respectively.) In the practolol group, but not the propranolol group, the duration of the atrial intracellular potentials was prolonged. There was no evidence that the prolonged treatment with either drug had a negative inotropic effect, or reduced positive inotropic responses to isoprenaline.

Animals↗