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PubMed1986

Effects of propranolol and nifedipine on exercise-induced attack in patients variant angina: assessment by exercise thallium-201 myocardial scintigraphy with quantitative rotational tomography.

To examine the effects of propranolol and nifedipine on exercise-induced attack in patients with variant angina, exercise 201Tl myocardial scintigraphy with quantitative analysis by emission-computed tomography was performed in 20 patients with variant angina after oral propranolol (80 mg), nifedipine (20 mg), and placebo. Exercise-induced attack occurred in 11 patients on placebo, in 14 on propranolol, and in none on nifedipine. The exercise duration was significantly shorter in those on propranolol (p less than .05), but significantly longer in patients on nifedipine (p less than .05) than in those on placebo. The peak rate-pressure product was significantly lower in patients on propranolol (p less than .01), but did not change in those on nifedipine, as compared with that in patients on placebo. The size of the perfusion defect as measured by 201Tl tomography was significantly greater in patients on propranolol (p less than .05), but significantly less in those on nifedipine (p less than .01) than in those on placebo. In conclusion, propranolol does not suppress but rather may aggravate exercise-induced attack in patients with variant angina, while nifedipine suppresses it. This unfavorable effect of propranolol on exercise-induced attack in patients with variant angina is likely to be due to a reduction of regional myocardial blood flow.

Adult↗
PubMed1975

Altered renin release and propranolol potentiation of vasodilatory drug hypotension.

Vasodilating antihypertensive drugs induce hypotension with reflex tachycardia, renin release, and fluid and electrolyte retention. Propranolol can impair this renin release. The studies described here were designed to determine the hemodynamic role of vasodilatory drug-induced renin release and inhibition thereof by propranolol in two animals models, the unanesthetized, normotensive and the unanesthetized, genetically hypertensive rat. In studies with normotensive rats, propranolol impaired renin release and tachycardia resulting from hydralazine and minoxidil and potentiated their hypotensive action. Two additional interventions against the renin-angiotensin system were used in evaluating the mechanism of this potentiation. One was removal of the renin source by nephrectomy, and the second was blockade of angiotensin's vasoconstrictor action using a selective angiotensin antagonist, saralasin (1-Sar-8-Ala-angiotensin II (previously known as P113)).. Both interventions potentiated vasocilatory drug hypotension, as did propranolol, but did not prevent reflex tachycardia. When combined with saralasin propranolol did not add to protentiation by this peptide. A similar pattern of blood pressure decrement and potentiation was seen in genetically hypertensive rats when propranolol or saralasin treatment preceded hydralazine. Propranolol was demonstrated to block hydralazine-induced increases in serum renin activity in genetically hypertensive rats. We conclude that hypotensive potentiation of vasocilating drugs by propranolol in these animal models is mediated to a large extent by impairment of renin release. Persistence of hypotensive tachycardia after nephrectomy and after saralasin in normotensive rats suggests the irrelevance of angiotensin's central nervous system stimulation to this cardiac effect. Clinical studies are underway to quantify the potential importance of this beneficial drug interaction in man.

Angiotensin II↗
PubMed1979

beta-Blockade therapy for supraventricular tachyarrhythmias after coronary surgery: a propranolol withdrawal syndrome?

A high incidence of cardiac arrhythmias and hypertension has been noted after coronary artery bypass surgery in patients previously treated with oral propranolol. Forty-two patients undergoing coronary bypass surgery had propranolol withdrawal 10 hours before surgery and were randomized into a group treated with propranolol immediately postoperatively, and a nontreatment group. Patients treated with prophylactic propranolol had a significantly lower incidence of postoperative supraventricular arrhythmias compared to patints who received no prophylaxis. All the arrhythmias responded rapidly to 1 mg of intravenous propranolol therapy, whether it was used as a primary treatment or as a supplement to prophylactic propranolol. The findings suggest that (1) there is a high incidence of supraventricular arrhythmias and sinus tachycardia after coronary artery bypass which might reflect an abrupt propranolol withdrawal, and (2) that perioperative prophylactic or supplementary propranolol therapy will successfully prevent or treat most of these arrhythmias.

Coronary Artery Bypass↗
PubMed1999

Studies on the pharmacokinetics and pharmacodynamics of propranolol in hyperlipidemia.

The lipophilic beta-adrenoreceptor antagonist propranolol has been studied to define its pharmacokinetic and pharmacodynamic characteristics in hyperlipidemic patients. A total of 48 subjects were allocated to four study groups: (1) healthy volunteers, (2) hypercholesterolemic patients, (3) hypertriglyceridemic subjects, and (4) patients with a mixed form of hyperlipidemia. Propranolol was given orally as a single dose of 80 mg. Heart rate was measured during 12 hours. At each point, the concentrations of propranolol were estimated. Moreover, heart rate and arterial systolic blood pressure were examined at rest and after a submaximal exercise test 3 hours after administration of propranolol (i.e., at the peak of propranolol concentration in the blood serum). A significant increase in the area under the serum concentration-time curve (AUC) by 39% and a reduction of the volume of distribution and total body clearance by 48% and 46%, respectively, without a significant change in the half-life time, were observed in patients with hypertriglyceridemia in comparison with the control group. The acceleration of exercise heart rate and the elevation of systolic blood pressure were comparable in all groups in the study, whereas blood serum concentrations of propranolol in patients with hypertriglyceridemia (group 3) and the mixed form of hyperlipidemia (group 4) were markedly altered from those observed in normolipemic subjects. No relationship between the concentration of propranolol and the heart rate in the group with hypertriglyceridemia was seen. In the light of this study, the authors suggest that lipid metabolism disturbances do not affect the pharmacodynamics of propranolol.

Adult↗
PubMed1989

Acute and chronic effects of propranolol and primidone in essential tremor.

We studied the acute and chronic effects of propranolol and primidone in essential tremor by administering long-acting propranolol (80 to 160 mg/d) and primidone (50 to 250 mg/d) to 50 patients. We evaluated patients at 1, 3, 6, 9, and 12 months after treatment and assessed tremor by subjective rating by patients, clinical scoring, and thermographic (accelerometer) recordings. Acute adverse reactions occurred in 8% with propranolol and 32% with primidone. Propranolol was without therapeutic effect in 30%, and 32% had no benefit from primidone. Significant chronic side effects occurred in 17% taking propranolol and in 0% with primidone. Tolerance to drug effect occurred with chronic treatment in 12.5% of patients with propranolol and 13.0% with primidone. We conclude that propranolol and primidone are effective long-term treatment for some patients with essential tremor. Acute adverse reactions with primidone and side effects with chronic use of propranolol hamper therapy.

Aged↗
PubMed1988

Application of propranolol to the keratinized oral mucosa: avoidance of first-pass elimination and the use of 1-dodecylazacycloheptan-2-one (Azone) as an absorption enhancer of bioadhesive film-dosage form.

The bioavailability of propranolol applied to the oral mucosa was examined in the hamster. The capacity of hamster cheek pouch, used as a model of keratinized oral mucosa, to metabolize propranolol in vitro is enormously lower than that of the liver. Significant amounts of propranolol absorbed from the small intestine were metabolized to naphthoxylactic acid and 4-hydroxypropranolol (4HP) during the passage through the intestinal wall, and then the greater portion of unchanged propranolol and almost all 4HP were subsequently metabolized by hepatic first-pass elimination in vivo. The systemic bioavailabilities of propranolol after the intra-small-intestinal loop and the intra-cheek-pouch administrations were 8.4% and 88.5%, respectively. The bioavailability of propranolol was improved further (to 97.1%) by a 1-h pretreatment of the cheek pouch with 5% 1-dodecylazacycloheptan-2-one (Azone)-emulsion. Bioadhesive film-dosage forms of propranolol were prepared with hydroxypropylcellulose. Both the in vitro permeation and the in vivo absorption of propranolol across the cheek pouch were enhanced by the incorporation of Azone to the film-dosage form.

Absorption↗
PubMed1990

Effects of betaxolol on cardiohemodynamics and coronary circulation in anesthetized dogs: comparison with atenolol and propranolol.

Effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on cardiohemodynamics and coronary circulation were investigated in two kinds of anesthetized open-chest dog preparations in comparison with those of atenolol and propranolol. When administered intravenously, betaxolol, atenolol and propranolol produced dose-dependent decreases in the heart rate (HR), maximum left ventricular dP/dt [+)dP/dt), cardiac output (CO) and mean arterial pressure (MAP). Although all three drugs were almost equipotent in decreasing HR, betaxolol was much less potent than atenolol and propranolol in decreasing (+)dP/dt. Betaxolol decreased the total peripheral resistance (TPR), whereas atenolol and propranolol increased it. In another series of experiments, when administered intravenously, betaxolol, atenolol and propranolol all produced a decrease in the myocardial oxygen consumption (MVO2) and an increase in the atrioventricular conduction time (AVCT). All three drugs were nearly equipotent in decreasing MVO2, although betaxolol was less potent than the other two drugs at higher doses (greater than 300 micrograms/kg). Prolongation of AVCT with propranolol was stronger than those with betaxolol and atenolol. These results suggest that, unlike atenolol and propranolol, the decrease in TPR as well as beta 1-adrenoceptor blockade may be responsible for both the hypotensive effect of betaxolol and the decrease in MVO2 with betaxolol. The result that the cardiodepressant effect of betaxolol was much less potent than those of atenolol and propranolol suggests that betaxolol would be more beneficial than the others in the treatment of ischemic heart disease.

Animals↗
PubMed1989

Propranolol in the primary prevention of upper gastrointestinal tract haemorrhage in patients with cirrhosis of the liver and oesophageal varices.

A prospective, randomised, multicentre, single-blind comparison of propranolol with placebo in the primary prevention of upper gastrointestinal haemorrhage was conducted in 230 cirrhotic patients with large oesophageal varices. The dose of propranolol was progressively increased until resting heart rate was reduced by 20 to 25%. The final doses were 40 mg of conventional propranolol and 160 and 320 mg of long-acting propranolol daily in 22, 60 and 18% of patients, respectively. Patients who survived without bleeding were followed up for 436 +/- 172 days (mean +/- SD). After 2 years, the cumulative percentages of patients free from bleeding were 74% in the propranolol group and 39% in the placebo group (p less than 0.05). Similarly, cumulative 2-year survival was 72% in the propranolol group and 51% in the placebo group (p less than 0.05). Propranolol was well tolerated and only 13 patients were withdrawn from treatment. We concluded that propranolol treatment decreased the incidence of first bleeding and death during a period of 2 years in patients with cirrhosis and large esophageal varices.

Aged↗
PubMed1983

Propranolol in pregnancy three year prospective study.

We compared propranolol with methyldopa in a randomized prospective study of 28 women with pregnancy associated hypertension. Both drugs were equally effective in controlling maternal hypertension. There was no significant difference in the birthweights of the babies in each group. However one infant born to a mother receiving propranolol had symptomatic hypoglycaemia. The mean peak levels of propranolol, propranolol glucuronide, 4-hydroxypropranolol, and 4-hydroxypropranolol glucuronide were not significantly different in the first, second, third trimesters and at least 3 months post partum. The mean peak plasma level of naphthoxylactic acid however was significantly less in the third trimester compared with post partum levels. Propranolol and its metabolites were found to cross into breast milk with the maximum dose likely to be ingested by the infant as either propranolol or propranolol glucuronide being 7 micrograms of propranolol per 100 g of breast milk, being approximately 0.1% of the maternal dose.

Blood Pressure↗
PubMed1999

Impaired results of a randomised double blinded clinical trial of propranolol versus placebo on the expansion rate of small abdominal aortic aneurysms.

BACKGROUND: To study the propranolol treatment of small abdominal aortic aneurysms (AAA) concerning intention to treat, side effects, and inhibition of expansion. METHODS DESIGN: Two-year lasting prospective randomised double-blinded intervention trial. SETTING: Hospital-based mass screening for AAA with annual ambulatory control of small AAA. PARTICIPANTS: Of 122 screening-diagnosed small AAA, 51 (42%) were excluded because of contraindications or present beta-blockage, and 17 refused participation. Thus, 54 (44.3%) were included. INTERVENTION: Participants were randomised to 40 mg propranolol twice a day or placebo. MEASURES: The same observed was used to follow-up AAA-expansion, side effects, quality of life (QL), branchial and ankle blood pressure (ABI), and pulmonary function (FEV1 and FVC). RESULTS: Sixty percent in the propranolol group, and 25% in the placebo group dropped out, mainly caused by dyspnoea in the propranolol group (RR=1.74, 95% C.I.: 1.06-2.86). Five (16.7%) died in the propranolol group, while 1 (4.2%) died in the placebo group (RR=1.6 (1.02-2.51)). Furthermore, decreased pulmonary function, ABI, and QL was noticed in the propranolol group. Consequently, the trial was stopped after two years. Ninety-five percent of the measurements of the AAA were measured within 2 mm variation. If expansion was defined as above 2 mm annually, the relative risk of expansion in the placebo group was 1.17 (0.74-1.85), and 2.44 (0.88-6.77) among the non-drop-outs. CONCLUSIONS: Only 22% of small screenings-diagnosed AAA were treatable with propranolol for two years. Consequently, only large scale studies are capable of showing potential minor inhibition of expansion by propranolol. However, whether such treatment ever becomes ethically acceptable is debatable.

Adrenergic beta-Antagonists↗
PubMed1999

[Effect of hydroxylation polymorphism on the concentration of propranolol in the blood of humans with hyperlipidemia].

An influence of hydroxylation phenotype on the concentration of propranolol [corrected] was examined in 52 subjects with hyperlipidemia divided into 4 groups: 1--control, normolipemic, 2--hypercholesterolemic, 3--hypertriglyceridemic, and 4--mixed-form hyperlipidemic. Each study group included extensive metabolizers and one subject characterized by a poor hydroxylation phenotype. Propranolol was given intragastrically at a single dose of 80 mg [corrected]. Blood was sampled within 24 hours following the drug administration. HPLC method was used for determining blood serum concentrations of propranolol. In each study group mean blood serum concentrations of propranolol in poor metabolizers were at maximum in subject with hypertriglyceridemia, at minimum in the normolipemic one, and intermediate in hypercholesterolemic (upper) and mixed-form hyperlipidemic ones. Lipid metabolic disturbances also affected blood serum concentrations. They were the highest in hypertriglyceridemic patients, whereas in hypercholesterolemic were, in early stage of observation, even lower then in normolipemic subjects. Blood serum concentrations of propranolol [corrected] attained minimal values in patients with mixed form of hyperlipidemia. In the light of the present study we can state that hyperlipidemia modifies the blood serum concentrations of propranolol [corrected]. Although, the type of hyperlipidemia and lipophilic propranolol are not the only determinants affecting blood serum concentrations of propranolol, but also a genetic factor, i.e. hydroxylation phenotype may play an important role.

Adolescent↗
PubMed2000

CYP1A2 and CYP2D6 4-hydroxylate propranolol and both reactions exhibit racial differences.

We have previously shown racial differences in propranolol kinetics, with the largest differences appearing to be in its 4-hydroxylation. The purpose of this study was to identify and confirm the cytochrome P450 enzymes (CYP) with propranolol 4-hydroxylase activity, describe their enzyme kinetics, and determine whether there were racial differences in their catalytic activity. Eleven human recombinant, expressed CYPs were screened, but only CYP1A2 and CYP2D6 possessed propranolol 4-hydroxylase activity. Subsequent studies were conducted in human liver microsomes, including correlation, inhibition, enzyme kinetics, and racial comparison studies. Significant correlations were noted between propranolol 4-hydroxylation and ethoxyresorufin-O-deethylation (marker of CYP1A2 activity), with marked improvement in the correlations when CYP2D6-mediated propranolol 4-hydroxylation was inhibited with quinidine. Inhibition studies showed that quinidine inhibited approximately 55% of propranolol 4-hydroxylation and furaphylline (CYP1A2-selective inhibitor) inhibited about 45% of propranolol 4-hydroxylation. Median (range) parameter estimates of (S)-4-hydroxypropranolol [(S)-HOP] formation were a V(max) value of 307 (165-2397) and 721 (84-1975) pmol/mg of protein/60 min for CYP1A2 and CYP2D6, respectively, and a K(m) value of 21.2 (8.9-77.5) and 8.5 (5.9-31.9) microM for CYP1A2 and CYP2D6, respectively. CYP1A2- and CYP2D6-mediated propranolol 4-hydroxylation was about 70 and 100% higher (P <.05 for both), respectively, in African-Americans compared with Caucasians. In summary, we found that both CYP1A2 and CYP2D6 catalyze formation of 4-hydroxypropranolol and that both enzymes exhibited racial differences in this reaction. The observed racial differences in drug metabolism may have relevance to drug efficacy, toxicity, or carcinogen activation for CYP1A2 or CYP2D6 substrates.

Aryl Hydrocarbon Hydroxylases↗
PubMed1975

Interaction between halothane and propranolol on oxytocin-induced uterine contractions.

Halothane and other volatile anesthetics were found to relax uteri maximally contracted by oxytocin and to enhance the relaxant effect of propranolol and other agents (tetracaine, quinidine and chlorpromazine) with local anesthetic properties. Concentration-effect curves for inhibition by propranolol or tetracaine were shifted to the left by halothane. Methoxyflurane, chloroform and diethyl ether also increased the effect of propranolol. The tissue/medium ratio for propranolol was increased by halothane. The uptake of propranolol was saturable and was decreased at 2.5 degrees C, suggesting an active transport mechanism. The increased uptake of propranolol in the presence of halothane was probably insufficient to account for the synergism noted. Inhibition by propranolol and tetracaine was inversely related to the concentration of calcium in the medium. The inhibitory effect of propranolol, tetracaine, quinidine and chlorpromazine appeared to be related to their ability to inhibit calcium transport.

Anesthetics↗
PubMed2001

Propranolol increases phosphatidic acid level via activation of phospholipase D.

AIM: To investigate the propranolol-induced phospholipase D (PLD) activity, its contribution to the increase in the level of phosphatidic acid, and the role of protein kinase C (PKC) in this event. METHODS: A combination of [3H]-myristate labeling, transphosphatidylation reaction, lipid extraction, and thin layer chromatography was used to measure the PLD activity. PKC inhibitors and prolonged phorbol-12-myristate-13-acetate (PMA) treatment were used to study the involvement of PKC in propranolol-induced PLD activation. Immunoblotting was used to detect the intracellular levels of PKC. RESULTS: Treatment of A-549 cells with propranolol in the presence of butanol, resulted in the rapid activation of PLD. Propranolol induced the formation of phosphatidylbutanol (PBut), a unique product of PLD, at the expense of phosphatidic acid (PA) formation. Pretreatment of cells with PKC inhibitors Ro-31-8220, staurosporine, and rottlerin increased the propranolol-induced PLD. Down-regulation of PKC by prolonged treatment of cells with PMA also potentiated the propranolol-induced PLD activity. CONCLUSION: Propranolol induces rapid activation of PLD activity, which results in the increase in intracellular level of PA. The data also indicate that propranolol-induced PLD activity could be negatively regulated by PKC.

Enzyme Activation↗
PubMed1979

Pharmacokinetics of propranolol in the cat and comparisons with humans and three other species.

The aims of this study were to describe the pharmacokinetics of propranolol in the cat, to compare pharmacokinetic parameters for propranolol in the cat with those of four other species and to apply the two-step infusion method of Wagner (Clin. Pharmacol. Ther. 16, 691-700, 1974) in order to attain a rapid steady-state level for propranolol in plasma. Seven healthy adult cats received propranolol either as an I.V. bolus or by the two-step I.V. infusion method. The latter method was very effective in rapidly attaining and maintaining steady-state plasma propranolol levels. Pharmacokinetic parameters for propranolol in the cat are as follows: plasma clearance, 31.3 ml/(kg x min); volume of distribution, 1.57 L/kg; elimination half-life, 35 min. When compared with other species, the order of plasma clearances for propranolol were: rat greater than dog greater than cat greater than man greater than monkey. A plot of total area under the plasma propranolol concentration-time curve versus dose was not linear at the lower doses, but was linear at doses greater than 0.242 mg/kg.

Animals↗
PubMed1976

Effects of propranolol on haemodynamic changes and gas exchange at rest, in orthostasis, and on exercise in patients with arterial hypertension.

The effects of propranolol on the circulation and respiration were studied in 38 patients with essential hypertension and symptomatic renal hypertension. The hypotensive effect of propranolol was associated with decrease in the cardiac index and heart rate; the peripheral vascular resistance moderately increased, and the circulating blood volume and haematocrit value showed no essential changes. Besides, a prolongation of the pre-ejection period, the decrease of intrasystolic index, an increase in the myocardial wall-tension index, and a retardation of the elevation rate of the intraventricular pressure were observed. After propranolol medication, on transition into the vertical position the heart rate showed a less marked acceleration; the remaining haemodynamic parameters changed in orthostasis as they had done before the treatment. After propranolol medication, on exercise the systolic and mean arterial pressures, heart rate, and cardiac output exhibited lesser increases than before the treatment, whereas the circulating blood volume, diasolic pressure, and peripheral vascular resistance increased just as they had done before the treatment. At rest, during propranolol medication there appeared a certain tendency to decreased oxygen uptake; in orthostasis the degree of increase in oxygen uptake did not change by the action of propranolol. Besides, propranolol did not alter the blood-plasma levels of lactic acid and pyruvate at rest and did not essentially change the oxygen uptake during exercise. The level of lactic acid and the lactate/pyruvate quotient in plasma during exercise increased slightly less after than without propranolol.

Blood Volume↗
PubMed1992

Metoprolol and propranolol treatment in carbon tetrachloride-induced hepatic injury.

The effects of beta 1-selective metoprolol (CAS 37350-58-6) and the nonselective beta-adrenoceptor antagonist propranolol (CAS 525-66-6) were investigated in healthy and CCl4 damaged male rats. Treatments were performed for 16 days, orally with dosages reducing heart beat/min by 25% (metoprolol 10 mg/kg, propranolol 1 mg/kg). Liver glycogen content was not influenced by either beta-blocker in healthy animals. CCl4-induced loss of glycogen was equally moderated by metoprolol and propranolol. Blood glucose increased in metoprolol treated healthy and liver damaged rats after a single dosage likewise following prolonged treatment. Propranolol was without effect on blood glucose level. Cytochrome P-450 decline in microsomal fraction was greater in metoprolol, than in propranolol treated healthy animals. However, the severe fall elicited by liver injury was moderated by metoprolol and normalised by propranolol. Cytochrome b5 seems to be involved in metoprolol metabolism. Cytochrome P-450-dependent aminopyrine-N-demethylase was impeded by metoprolol in animals with healthy liver. The serious inhibition caused by CCl4 was moderated by metoprolol and with a better result by propranolol. The high serum bilirubin level in liver lesion was lowered by metoprolol and particularly by propranolol. Neither phase I metabolic process aminopyrine-N-demethylation nor phase II glucuronidation were normalised. A comparison of this data with the results of a previous 12-day treatment schedule indicates that no changes in efficacy occurred with longer treatment. The present results pertain to the importance of the selection of beta-adrenoceptor blocker in liver lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine N-Demethylase↗
PubMed2005

The effect of a combined treatment with propranolol and isosorbide-5-mononitrate on Doppler ultrasound parameters in patients with cirrhosis and portal hypertension.

OBJECTIVES: The objectives of this study were to compare the effect of the treatment with propranolol to that with propranolol and isosorbide-5-mononitrate in portal hypertension, as assessed by Doppler ultrasound parameters in patients with cirrhosis. METHODS: A prospective study of two groups, each of 30 patients with cirrhosis Child-Pugh A was performed. In one group 40 mg/day propranolol were administered for 6 months and in the other, a combined treatment with propranolol 40 mg/day and isosorbide-5-mononitrate 40 mg/day was administered for 6 months. In all patients the presence of esophageal varices was confirmed by upper gastrointestinal endoscopy and abdominal ultrasonography and Doppler ultrasonography of the portal vein was performed. The patients were monitored for: the velocity of blood flow in the portal vein, the cross sectional area of the portal vein and the portal vein congestion index. Data analysis used t-Student test, Pearson and Spearman correlation. A p value of <0.05 was considered to be significant. RESULTS: A significant decrease of all parameters after 6 months was observed in the group with combined therapy with propranolol and isosorbide-5-mononitrate (p<0.05). The relative decrease of the cross sectional area of the portal vein and of the portal vein congestion index was more important when patients had higher initial values of the two parameters, indicating an increased hemodynamic impairment (Pearson, p<0.001). In patients treated only with propranolol, the relative decrease correlated with its initial value for all parameters. CONCLUSION: The combined therapy with propranolol and isosorbide-5-mononitrate proved to be superior to the mono-therapy with propranolol in decreasing the hemodynamic parameters in portal hypertension, probably by an additive effect.

Adrenergic beta-Antagonists↗