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PubMed1976

Propranolol and morphine.

The morphine blocking and anticonvulsant effects of propranolol were investigated in mice. Three different convulsant procedures (electroshock, pentylenetetrazol and thebaine) were used. In addition, LD50's of morphine after different doses of propranolol were done. Sotalol was used as a control drug to check which of the effects of propranolol could be regarded as due to beta blockade. Morphine LD50 in mice is not altered by pre-treatment with propranolol. The anticonvulsant characteristics of propranolol are different from those of sotalol, the former acting mainly on the tonic phase of the seizures. This study does not support the hypothesis that propranolol is a morphine antagonist but reinforces the idea that propranolol has definite central nervous system effects.

Animals↗
PubMed1979

The influence of (+)-propranolol on the inotropic effect of dihydro-ouabain in relation to stimulation frequency.

1. The influence of (+)-propranolol, 10(-6) to 4 x 10(-5) mol/l, upon the positive inotropic effect of dihydro-ouabain was studied on guinea-pig papillary muscle. At 1 Hz, negative inotropically effective concentrations of (+)-propranolol decreased the inotropic effectiveness of the glycoside. 2. For equivalent diminution of the basal force of contraction, either by reduction of stimulation frequency or by increasing concentrations of (+)-propranolol, a similar decrease in the inotropic effectiveness of dihydro-ouabain was observed. In contract, reduction of [Ca2+]o had almost no effect on the effectiveness of the glycoside. 3. The inhibitory effect of (+)-propranolol on the inotropic effectiveness of dihydro-ouabain declined with reduction of stimulation frequency. At any stimulation frequency tested, the inhibitory effect of (+)-propranolol was proportional to the effect of a reduction of that particular frequency to the rested-state condition in the absence of (+)-propranolol. 4. The results are consistent with the hypothesis that the inhibition of the excitation-coupled sodium influx by (+)-propranolol is the cause of its inhibiting effect on the effectiveness of dihydro-ouabain.

Animals↗
PubMed1982

Pharmacokinetics of propranolol and sotalol in hyperthyroidism.

The elimination and bioavailability of two beta-blocking agents, propranolol and sotalol, were studied in 10 thyrotoxic patients, both before and after treatment with iodine-131. Each subject received in random order propranolol 160 mg and sotalol 160 mg as single oral doses both while hyperthyroid and after euthyroidism had been achieved. The pharmacokinetics of sotalol was not affected by hyperthyroidism, whereas serum propranolol concentrations were significantly lower during hyperthyroidism than in the euthyroid state. During hyperthyroidism, the bioavailability of propranolol was significantly reduced (p less than 0.05) and its clearance was increased (p less than 0.005), whereas there was no difference in its serum t 1/2. This indicates that the bioavailability of propranolol in hyperthyroidism is reduced by a mechanism which may depend on increased first-pass metabolism in the liver, or on an increased distribution volume of the drug. Both propranolol and sotalol caused a slight decrease in serum tri-iodothyronine concentration. As the effects of beta-blocking agents on the symptoms of hyperthyroidism are correlated with the serum concentration of the drugs, sotalol, with its long half-life and unaltered elimination in hyperthyroidism, has certain advantages over propranolol in the treatment of thyrotoxicosis.

Adult↗
PubMed1989

Modulation of the effects of salbutamol by propranolol and atenolol.

Six healthy volunteers were given single oral doses of 8 mg salbutamol, 40 mg propranolol, 100 mg atenolol, 8 mg salbutamol plus 40 mg propranolol and 8 mg salbutamol plus 100 mg atenolol, in a placebo controlled study. Plasma potassium fell following salbutamol and rose following atenolol or propranolol, and the hypokalaemic effect of salbutamol was reversed more effectively by propranolol than by atenolol. Although blood glucose rose after salbutamol, it was unaffected by any of the other treatments. Lying and standing pulse rate rose after salbutamol and fell equally after either beta-adrenoceptor antagonist, and fell more after salbutamol plus propranolol than after salbutamol plus atenolol. Blood pressure rose after salbutamol and fell after each of the other treatments. Forty milligrams propranolol was thus more effective than 100 mg atenolol in reversing the metabolic effects of 8 mg salbutamol, and was as effective in reversing the cardiovascular effects. In cases of symptomatic salbutamol overdose, propranolol should be considered as an antidote provided the patient is not asthmatic.

Adult↗
PubMed1981

Pharmacokinetics and pharmacodynamics of propranolol stereoisomers in hyperthyroid patients.

The disposition of propranolol stereoisomers after administration of a single oral dose of the racemic drug was investigated in seven hyperthyroid patients before and after antithyroid drug therapy. The possibility of hypersensitivity to propranolol in the patients was evaluated by constructing plasma propranolol concentration -- beta-blocking effect curves. There was no statistically significant difference in elimination half-life (t1/2) between (+/-)- and (-)-propranolol before and after antithyroid drug therapy. However, the plasma clearance (Vp) of (-)-propranolol was smaller than that of (+/-)-propranolol, and the difference was statistically significant after antithyroid drug therapy. Vp decreased or did not change in young patients after therapy. No significant difference was observed in the relationship between the tilt-induced pulse rate response and plasma propranolol concentration when treated patients became euthyroid compared to their response in the hyperthyroid state.

Adult↗
PubMed1978

Effects of propranolol and oxprenolol on the vasoconstrictor response to noradrenaline in the superficial hand vein in man.

The effects of oxprenolol and propranolol on the venoconstrictor response to noradrenaline were studied in healthy volunteers by measuring superficial dorsal hand vein diameter at a standard congesting pressure. In 8 subjects dose response curves to noradrenaline (20-1280 ng/ml) were obtained with noradrenaline alone, with noradrenaline plus propranolol 10 microgram/ml, with noradrenaline plus propranolol 10 microgram/ml plus oxprenolol 3 microgram/ml and with noradrenaline plus propranolol 13 microgram/ml according to a double blind balanced randomised design. Propranolol 10 microgram/ml significantly (p less than 0.05) potentiated the vasoconstrictor response to noradrenaline and the addition of oxprenolol significantly (P less than 0.05) reversed the potentiation giving a response similar to that seen with noradrenaline alone. The higher concentration of propranolol did not produce further potentiation, the response being similar to that obtained with the lower concentration of propranolol. It is suggested that the effect of oxprenolol may be attributable to alpha blocking properties, to partial beta agonism or to its membrane stabilising properties.

Drug Interactions↗
PubMed1986

Peripheral vascular effects of bufuralol in hypertensive and normal subjects: a comparison with propranolol and pindolol.

In a double-blind, single oral dose, cross-over study, the effects of bufuralol (60 mg) on heart rate, blood pressure, and peripheral vascular responses were compared with those of propranolol (160 mg), pindolol (10 mg), and placebo in a group of 12 healthy volunteers. All three beta-adrenoceptor antagonists reduced exercise tachycardia, but at the doses chosen the effects of bufuralol were less than those of propranolol. Forearm blood flow was reduced by propranolol and pindolol, but not by bufuralol. The antihypertensive and peripheral vascular effects of bufuralol (30-60 mg bd) were also compared with those of propranolol (40-80 mg bd) in a double-blind crossover study in 10 patients with mild hypertension. Propranolol and bufuralol produced comparable reductions in systemic blood pressure over a two-week period, but the decreases in forearm and finger blood flow were greater with propranolol. These studies suggest that bufuralol is a beta-adrenoceptor antagonist with antihypertensive properties, and that it produces less peripheral vasoconstriction than propranolol or pindolol.

Adult↗
PubMed1988

A comparison of felodipine and propranolol as additions to hydrochlorothiazide in the treatment of hypertension.

Eighty one patients with uncomplicated hypertension who required additional antihypertensive medication (diastolic Phase V [dBP] greater than or equal to 95 mm Hg) after 4 weeks treatment with hydrochlorothiazide (HCTZ) 25 mg o.m. were randomized to receive felodipine 5 mg b.i.d. (n = 40) or propranolol (n = 41) 80 mg b.i.d. in addition to HCTZ 25 mg o.m. If the dBP measured about 12 h post-dose was not less than or equal to 90 mm Hg after 4 weeks, the dose of felodipine or propranolol was doubled. The double blind trial period was 8 weeks for all patients. Over the 8 week period, felodipine reduced the seated dBP from 100 to 83 mm Hg and propranolol from 101 to 86 mm Hg. The attained seated dBPs were significantly different in the two groups. About one third of patients in each group received the high dose of second-line therapy. After 8 weeks 91% of patients receiving HCTZ+felodipine and 84% receiving HCTZ+propranolol had a dBP less than or equal to 90 mm Hg. Both regimens were well-tolerated with an equal incidence but different pattern of adverse events (felodipine: flushing, headache and peripheral oedema; propranolol: dyspepsia, fatigue and vasospasm). In this 8-week study, felodipine and propranolol were safe and effective second-line antihypertensive drugs when added to hydrochlorothiazide. At the doses selected, felodipine was at least as effective as propranolol.

Adult↗
PubMed1985

Effects of (+)-propranolol on intracellular mechanisms of contraction in striated muscle of the rabbit.

In functionally skinned muscle fibers from the rabbit, we studied the effect of propranolol on calcium activation of the contractile proteins and, in separate experiments, on calcium uptake and release from the sarcoplasmic reticulum (SR) while measuring physiological tension. Pieces from isolated papillary muscle (PM), soleus (SL) (slow-twitch skeletal muscle), and adductor magnus (AM) (fast-twitch skeletal muscle) were homogenized (sarcolemma disrupted). A fiber bundle from PM and single fibers from SL and AM were dissected from the homogenate and mounted on a photodiode tension transducer. To study Ca2+-activated tension development of the contractile proteins, we used high EGTA (7 mmol/l) to control the free calcium concentration. To study SR function, we used five different solutions to load the calcium into the SR and to release it from the SR with 25 mmol/l caffeine, thus producing a tension transient. In general, propranolol has similar mechanisms of action in the three muscle types. Propranolol (0.1-1.0 mmol/l) increased the submaximal calcium-activated tension development in all muscles but with PM = SL greater than AM, and this increase was correlated with increases in calcium binding to isolated troponin C. Propranolol increased the maximal calcium-activated tension development in PM and SL, but decreased that in AM. Propranolol at concentrations of 0.3-1.0 mmol/l decreased calcium uptake by the SR but did not change calcium release in any of the three muscles. In PM, however, propranolol at a concentration of 0.1 mmol/l increased calcium uptake by the SR. We conclude that propranolol induces decreases in muscle contraction mainly by decreasing calcium uptake by the SR.

Animals↗
PubMed1987

The effects of prazosin and propranolol in combination with thiazide diuretics on blood pressure and serum lipids: a multicentre study.

We have carried out randomized 12-week multicentre study to compare the effects of prazosin and propranolol on blood pressure and serum lipids in 70 patients with essential hypertension after a 4 week minimum period of treatment with thiazide diuretics. After 12 weeks treatment with prazosin (n = 40, 1.5-12.0 mg per day) or propranolol (n = 30, 30-120 mg per day) with diuretics there was a significant blood pressure reduction from 165.1/97.9 mmHg to 151.2/90.6 mmHg and from 167/96.5 mmHg to 153/91.9 mmHg, respectively. In the 12th week a significant decrease was noted in triglyceride and in low-density lipoprotein cholesterol (LDL + VLDL-C), but no significant effects were seen in high-density lipoprotein cholesterol (HDL-C) in patients receiving prazosin. On the other hand, a significant decrease in lecithin cholesterol acyltransferase (LCAT) was seen in patients receiving propranolol. Twenty-six of 40 patients receiving prazosin were given an additional 12 weeks of treatment. Twenty-two of 30 patients initially treated with propranolol were switched from propranolol to prazosin after 13 weeks and given prazosin up to the 24th week. At 24 weeks, the blood pressure was 149/93.0 mmHg in the prazosin group and 155/89.2 mmHg in the group which switched from propranolol to prazosin. Triglyceride remained reduced in the prazosin group at the 24th week. In the group which switched from propranolol to prazosin, triglyceride decreased significantly over the next 12 weeks.

Benzothiadiazines↗
PubMed1983

Divergent effects of atenolol, practolol and propranolol on the peripheral metabolic changes induced by dynamic exercise in healthy men.

A study has been made of the effects of intravenous atenolol, practolol and propranolol on the changes induced by exhaustive dynamic physical exercise in blood pressure, heart rate and blood levels of lactate, glucose, insulin, free fatty acids and potassium. The mean endurance of dynamic exercise was reduced by all three beta-blockers, most markedly by propranolol. After all the beta-blockers heart rate showed a similar decrease during the first 60 min of exercise; atenolol caused the smallest reduction at exhaustion. All three beta-blockers lowered the systolic blood pressure during exercise; propranolol was the most active agent both during exercise and during recovery. The diastolic pressure was higher during exercise after treatment with the beta-blockers, especially propranolol. The beta-blockers did not markedly affect the elevation of blood lactate induced by exercise. The increase in blood glucose was abolished by atenolol. Plasma insulin was reduced by exercise after beta-blockade, most markedly after propranolol and practolol. All the beta-blockers were equipotent in reducing up to 60 min the exercise-induced increase in plasma free fatty acids, although at exhaustion propranolol had a significantly greater effect than atenolol or practolol. Serum potassium was higher after propranolol and atenolol than after practolol during exercise and recovery.

Adult↗
PubMed1986

Influence of propranolol coadministration or cigarette smoking on the kinetics of desmethyldiazepam following intravenous clorazepate.

The influence of propranolol coadministration or of cigarette smoking on the kinetics of desmethyldiazepam following a single 20-mg intravenous dose of clorazepate dipotassium was evaluated in healthy volunteers. In Study One, intravenous clorazepate was given once in the control condition, and again during coadministration of propranolol, 80 mg twice daily. Compliance with the prescribed propranolol regimen was verified by measurement of serum propranolol concentrations (mean, 37 ng/ml). In control vs propranolol treatment conditions, there was no significant difference in desmethyldiazepam volume of distribution (1.27 vs 1.23 liters/kg) or in free fraction in serum (1.83 vs 1.80% unbound). There was a small although statistically significant prolongation of desmethyldiazepam half-life (55 vs 61 h, P less than 0.05) and reduction in clearance (0.281 vs 0.247 ml/min/kg, P less than 0.02) attributable to propranolol. In Study Two, desmethyldiazepam kinetics were compared in eight cigarette smokers (mean, 19 cigarettes/day) and in 11 nonsmoking controls matched for age, sex, and body weight. There was no significant difference between controls and cigarette smokers in desmethyldiazepam volume of distribution (1.29 vs 1.34 liters/kg), elimination half-life (55 vs 59 h), clearance (0.284 vs 0.276 ml/min/kg), or free fraction in serum (1.96 vs 1.92% unbound). Thus, propranolol slightly although significantly impairs the clearance of desmethyldiazepam and prolongs its half-life. Cigarette smoking has no apparent influence on desmethyldiazepam kinetics.

Adult↗
PubMed1983

Effects of propranolol in vitro and in vivo on platelet function and thromboxane formation in normal volunteers.

In vitro and ex vivo effects of propranolol on platelet aggregation, formation of thromboxane B2 (TXB2) and platelet sensitivity to prostacyclin were studied in healthy men. Propranolol, added in vitro to platelet rich plasma (PRP) inhibited platelet aggregation and TXB2 formation induced by ADP, 1-epinephrine, collagen and arachidonic acid. Concentrations of 20-100 microM propranolol were effective when ADP, 1-epinephrine and collagen were used as stimuli. Higher concentrations (250-500 microM) were needed to inhibit aggregation induced by arachidonic acid. Oral administration of propranolol either as a single dose (120 mg) or for one week (3 x 40 mg/day) did, however, not affect platelet aggregation, thromboxane formation and platelet sensitivity to prostacyclin. In addition, withdrawal of propranolol was without effect on these parameters. Although propranolol has potent effects on platelet function in vitro, it seems that the blood levels achievable by oral administration of propranolol are too low to affect platelet aggregation and TXB2 formation.

Adult↗
PubMed1991

Propranolol pretreatment reduces cardiorespiratory toxicity due to plain, but not epinephrine-containing, intravenous bupivacaine in rats.

The purpose of this study was to evaluate the effects of pretreatment with propranolol on the cardio-respiratory toxicity of bupivacaine, either plain or with epinephrine 1:200,000 (5 micrograms.ml-1) added. Adult male Sprague Dawley rats, anaesthetized with intraperitoneal pentobarbital, were divided into four groups. Groups I and III were pretreated with iv propranolol 150 micrograms.kg-1, and Groups II and IV received iv NS as a placebo. Three minutes later, rats in Groups I and II received plain 0.5% bupivacaine, 4 mg.kg-1, and Groups III and IV received 4 mg.kg-1 of 0.5% bupivacaine with epinephrine, 5 micrograms.ml-1 iv. Five of eight rats pretreated with propranolol survived (Group I), compared with uniform fatality with NS pretreatment (Group II) (P less than 0.05). Addition of epinephrine to the bupivacaine eliminated the protective effect of propranolol. All rats pretreated with propranolol (Group III) or NS (Group IV) died when given bupivacaine with epinephrine. In conclusion, acute propranolol pretreatment reduced the fatal cardiotoxicity due to iv bupivacaine in male Sprague Dawley rats, but the addition of epinephrine 5 micrograms.ml-1 to bupivacaine eliminated the protective effect of propranolol.

Animals↗
PubMed2002

(-)-CGP 12177 increases contractile force and hastens relaxation of human myocardial preparations through a propranolol-resistant state of the beta 1-adrenoceptor.

Two forms of the activated beta1-adrenoceptor exist, one that is stabilized by (-)-noradrenaline and is sensitive to blockade by (-)-propranolol and another which is stabilized by partial agonists such as (-)-pindolol and (-)-CGP 12177 but is relatively insensitive to (-)-propranolol. We investigated the effects of stimulation of the propranolol-resistant beta1-adrenoceptor in the human heart. Myocardium from non-failing and failing human hearts were set up to contract at 1 Hz. In right atrium from non-failing hearts in the presence of 200 nM (-)-propranolol, (-)-CGP 12177 caused concentration-dependent increases in contractile force (-logEC50[M] 7.3+/-0.1, E(max) 23+/-1% relative to maximal (-)-isoprenaline stimulation of beta1- and beta2-adrenoceptors, n=86 patients), shortening of the time to reach peak force (-logEC50[M] 7.4+/-0.1, E(max) 37+/-5%, n=61 patients) and shortening of the time to reach 50% relaxation ( t(50%), -logEC50[M] 7.3+/-0.1, E(max) 33+/-2%, n=61 patients). The potency and maxima of the positive inotropic effects were independent of Ser49Gly- and Gly389Arg-beta1-adrenoceptor polymorphisms but were potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (-logEC50[M] 7.7+/-0.1, E(max) 68+/-6%, n=6 patients, P<0.0001). In the presence of (-)-propranolol and 3-isobutyl-1-methylxanthine, the potency (-logEC50[M] 7.4+/-0.1, P=0.0013, n=9 patients) but not the maximal effect of (-)-CGP 12177 was reduced in right atrium from failing hearts, which was associated with 64% and 52% reductions in the densities of low-affinity and high-affinity (-)-[3H]CGP 12177 binding sites. In the presence of (-)-propanolol and 3-isobutyl-1-methylxanthine, (-)-CGP 12177 increased atrial cyclic AMP levels and activated cyclic AMP-dependent protein kinase in right atrium from non-failing hearts. In right ventricle from failing hearts (-)-CGP 12177 increased contractile force (-logEC50[M] 7.4+/-0.1, E(max) 34+/-3%, n=13 patients) and hastened the time to peak force (-logEC50[M] 7.6+/-0.1) and time to reach 50% relaxation (-logEC50[M] 7.4+/-0.1) in the presence of (-)-propranolol and 3-isobutyl-1-methylxanthine. Our results show that (-)-CGP 12177 increases contractility and hastens relaxation through a cyclic AMP pathway in human myocardium, consistent with mediation through a (-)-propranolol-resistant state of the beta1-adrenoceptor. The reduction in heart failure of atrial inotropic potency of (-)-CGP 12177, as well as of the high-affinity and low-affinity binding sites for (-)-[3H]CGP 12177, is consistent with the beta1-adrenoceptor nature of these sites.

Adrenergic beta-1 Receptor Agonists↗
PubMed2002

Propranolol ameliorates thrombocytopenia in patients with cirrhosis.

BACKGROUND: Propranolol causes splanchnic arterial vasoconstriction owing to the unopposed alpha vasoconstriction resulting from the blockade of beta-2 adrenoceptors. It is therefore hypothesized that this drug may cause vasoconstriction in the splenic arterial circulation and, thus, modify the manifestations of hypersplenism, such as thrombocytopenia. The aim of the present study was to test this hypothesis. METHODS: Nineteen patients with cirrhosis and thrombocytopenia (fewer than thrombocytes 7 x 10(4)/mm3) were include. The subjects of the study. All of them were studied in the morning after an overnight fast. To evaluate splenic arterial hemodynamics, the pulsatility index was measured by Doppler ultrasonography. Platelet counts and platelet-associated immunoglobulin G levels were also recorded. The subjects were then randomized to receive propranolol (n = 10) or placebo (n = 9). The measurements were repeated after 1 week of propranolol or placebo administration. The dose of propranolol was determined so that a 20% to 25% reduction in heart rate was achieved. RESULTS: Placebo administration caused no significant changes in splenic artery hemodynamics. In contrast, propranolol administration significantly increased the intra splenic artery pulsatility index (from 1.10+/-0.06 to 1.24+/-0.08; P < 0.01). Placebo administration caused no significant changes in the platelet count. In contrast, propranolol administration significantly increased the platelet count (from 4.5+/-0.3 to 6.1+/-0.73 x 10(4)/mm3; P < 0.05). Furthermore, the change in platelet count was significantly correlated with either the change in extrasplenic artery pulsatility index (r = 0.78, P < 0.05) or the change in intrasplenic artery pulsatility index (r = 0.78, P < 0.01). Platelet-associated immunoglobulin G levels were not modified in either of the two groups. CONCLUSIONS: Propranolol ameliorates thrombocytopenia in patients with cirrhosis. This effect may be caused mainly by hemodynamic changes in the spleen, rather than being caused by immunological mechanisms.

Adrenergic beta-Antagonists↗
PubMed1982

Comparison of withdrawal phenomena after propranolol, metoprolol, and pindolol.

Three groups of hypertensive patients were studied after they had received one of the three pharmacologically different beta blockers for at least 1 month: pindolol, 10 mg twice a day (n = 7), propranolol median dose, 80 mg three times a day (n = 9), or metoprolol, 150 mg (twice a day (n = 8). After abrupt withdrawal of drug and replacement with placebo, we measured the following on day 0 and approximately every 2 days up to 3 weeks; beta-adrenergic sensitivity (BAS) by the chronotropic dose of isoproterenol to increase heart rate by 25 bpm (CD25), resting heart rate and blood pressure, and symptoms. All values are medians. On day 0, beta blockade was evident by increased CD25 values of 618 micrograms for pindolol, 57 micrograms for propranolol, and 10 micrograms for metoprolol as compared to 2.8, 2.4, and 3.0 microgram, respectively, at days 14 to 21, which were considered the ultimate baseline. After pindolol on day 0, the CD25 slowly decreased to, but never below, baseline by days 8 to 21. In contrast, after propranolol on day 0, the CD25 decreased significantly two- to fivefold below baseline from days 4 to 14 (BAS) and after metoprolol two- to threefold below baseline from days 2 to 8. After pindolol, heart rate and blood pressure gradually returned to, but not above, ultimate baseline. In contrast, during the period of BAS there was a significant overshoot of heart rate in eight patients after metoprolol (day 0 = 61, peak = 88, baseline = 74) but not after propranolol, while a significant overshoot of blood pressure occurred in six of nine patients after propranolol (day 0 = 140/87, peak = 157/95, baseline = 140/89) but not after metoprolol. Withdrawal symptoms of headache, palpitations, and tremor occurred in one of seven patients after pindolol, six of nine after propranolol, and three of eight after metoprolol. The degree and duration of beta blockade appeared related to drug potency. Withdrawal phenomena occurred after propranolol and metoprolol but not after pindolol.

Adult↗
PubMed1983

Double-blind comparison of trimazosin and propranolol in essential hypertension.

This report describes a double-blind, parallel, comparative study of trimazosin (+/- polythiazide) and propranolol (+/- polythiazide) in 130 patients with essential hypertension. Both treatment regimens were shown to be effective in achieving statistically significant sustained reduction in blood pressure. Propranolol alone was somewhat more effective, at the doses selected, than trimazosin alone, but the hypertension of nonresponders in each treatment group was effectively controlled by the addition of low doses of polythiazide. Trimazosin had no effect on heart rate, whereas propranolol significantly lowered resting heart rates, which was occasionally troublesome. Side effects were less frequent in the trimazosin-treated group. Trimazosin lowered serum creatinine and blood urea nitrogen, an effect significantly different from that of propranolol. There was also a tendency for serum uric acid to rise in patients receiving propranolol and fall in those receiving trimazosin; polythiazide significantly raised uric acid levels. The effects of trimazosin and propranolol on the lipid profile were small, but the difference between the increase in the high-density lipoprotein-cholesterol fraction in trimazosin-treated patients and the decrease in propranolol-treated patients was significant and thought to be of interest.

Adult↗