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PubMed1982

Ambulatory blood pressure during once-daily randomised double-blind administration of atenolol, metoprolol, pindolol, and slow-release propranolol.

Intra-arterial ambulatory blood pressure was measured over 24 hours, in 34 patients with newly diagnosed hypertension, both before and after double-blind randomisation to treatment with atenolol (n=9), metoprolol (n=9), pindolol (n=9), or propranolol in its slow-release form (n=7). The dosage of each drug was adjusted at monthly clinic visits until satisfactory control of blood pressure was achieved (140/90 mm Hg or less by cuff) or the maximum dose in the study protocol was reached. A second intra-arterial recording was made after these drugs had been taken once daily at 0800 for three to eight months (mean 5.0+/-SD 1.4) and was started four hours after the last dose.At the end of the 24-hour recordings blood pressure was significantly lower with all four drugs. The extent to which the drugs reduced blood pressure, however, differed over the 24 hours. Atenolol lowered mean arterial pressure significantly throughout all 24 recorded hours, metoprolol for 12 hours, pindolol for 15 hours, and slow-release propranolol for 22 hours. Neither metoprolol nor pindolol lowered blood pressure during sleep. A significant reduction in heart rate was observed over 20 hours with atenolol, 20 hours with metoprolol, 10 hours with pindolol, and 24 hours with slow-release propranolol. Atenolol, metoprolol, and slow-release propranolol continued to slow the heart rate 24 hours after the last tablet was taken; this effect on heart rate, however, was not sustained throughout the second morning in those patients taking atenolol. Pindolol, the only drug studied that has intrinsic sympathomimetic activity, increased heart rate and did not lower blood pressure during sleep.Atenolol and slow-release propranolol are effective as antihypertensive agents over 24 hours when taken once daily, whereas metoprolol and pindolol may need to be taken more frequently. At times of low sympathetic tone, however, such as during sleep, beta-blockers with intrinsic sympathomimetic activity may raise heart rate and attenuate the fall in blood pressure with treatment.

Adolescent↗

PubMed1983

Beta-blockers in bronchial asthma: effect of propranolol and pindolol on large and small airways.

In 11 asthmatic subjects the relative magnitude and the site of airway bronchoconstriction were compared after the oral administration of 40 mg of propranolol and 2.5 mg of pindolol and the magnitude and site of bronchodilation produced by 0.5 mg subcutaneous terbutaline were tested after pretreatment with propranolol and pindolol. Specific airway conductance (sGaw) and peak expiratory flow rate (PEFR), both believed to reflect changes in large airways, and capacity isoflow (Ciso-v) and delta Vmax50, both believed to reflect changes in small airways, were determined before and after administration of placebo, pindolol, and propranolol. Treatments were given double blind and in random order. After the administration of propranolol we noted a significant bronchoconstrictive effect in the large airways (mean values of PEFR and sGaw, expressed as percentages of control values, decreased by 87.4% +/- 13.2% and 43.3% +/- 8.9%) and in the small airways (mean value of Ciso-v increased by 20.6% +/- 4.7% and that of delta Vmax50 decreased by 50% +/- 11.9% of control). By contrast, pindolol produced no significant effect on sGaw or PEFR but the tests of small airway function showed significant bronchoconstriction (mean values of Ciso-v increased by 12.9% +/- 2.6% and those of delta Vmax50 decreased by 47.2% +/- 9.2%). This action makes pindolol potentially dangerous in asthmatic patients. The bronchodilator action of terbutaline on large airways is diminished after the use of both propranolol and pindolol.

Adult↗

PubMed1988

Pindolol, not propranolol, reverses cardiac hypertrophy in renal hypertensive rats.

Reversal of cardiac hypertrophy has been obtained by treatment with some antihypertensive drugs but has not been achieved consistently with beta blockers. To investigate whether this difference might be explained by the distinct hemodynamic actions of the drugs, we studied the effects of propranolol and pindolol, beta blockers with distinct modes of action, on cardiac hypertrophy of hypertensive male Wistar rats, two-kidney, one clip (2K1C) Goldblatt model (n = 33) and sham-operated control rats (n = 34). We also assessed the effects of such therapies on the ventricular pumping ability during open-chest, transient aortic occlusion. Four weeks after surgery, propranolol (5 mg/kg/day p.o.) was given to hypertensive (n = 8) and control rats (n = 11); pindolol was also given orally (1 mg/kg/day) to similar groups (n = 7 and n = 5, respectively). Untreated animals served as controls for both groups. Cardiac hypertrophy developed with hypertension in the untreated rats of the propranolol (3.38 +/- 0.18 vs 2.60 +/- 0.08 mg/g; p less than 0.01) and pindolol groups (3.93 +/- 0.21 vs 2.40 +/- 0.03 mg/g; p less than 0.001). Treatment reversed cardiac hypertrophy in the pindolol-treated (3.01 +/- 0.19 vs 3.93 +/- 0.21 mg/g; p less than 0.001, NS) but not in the propranolol-treated rats (3.24 +/- 0.18 vs 3.38 +/- 0.21 mg/g, NS). The maximal pressure that developed during aortic occlusion in the propranolol group was similar to that observed in the pindolol group. These results indicate that cardiac hypertrophy is reversed by pindolol but not by propranolol, and that this reversal does not interfere with left ventricular pumping ability.

Animals↗

PubMed1997

Effect of pindolol in hastening response to fluoxetine in the treatment of major depression: a double-blind, placebo-controlled trial.

OBJECTIVE: In two preliminary studies, pindolol produced robust results in hastening clinical response to antidepressant drugs in depressed patients. Validity of those pilot studies was limited by use of an open-label, unblinded study design, and so the authors conducted a double-blind, placebo-controlled trial to assess the effectiveness of pindolol in hastening response to fluoxetine. METHOD: Drug-free outpatients with major depression were concurrently treated with fluoxetine (20 mg/day) and either placebo or pindolol (5.0 mg b.i.d. or 2.5 mg t.i.d.), for 6 weeks, in a randomized, double-blind manner. After 6 weeks, all patients received fluoxetine and placebo and were followed for 3 further weeks in a single-blind manner. RESULTS: Forty-three patients completed at least 1 week of the protocol. Rates of partial remission after 2 weeks of treatment with fluoxetine and either pindolol or placebo were 17% (four of 23 patients) and 20% (four of 20 patients), respectively. At study completion, 65% of the patients (N = 28) demonstrated at least a partial remission, and there was no difference between treatment groups. The pindolol group, but not the placebo group, demonstrated significant reductions in blood pressure and pulse rate. The average time to remission and the rates of attrition, overall response, and side effects were similar in the two groups. CONCLUSIONS: These findings do not support the efficacy of pindolol in hastening clinical response in patients treated with fluoxetine.

Adolescent↗

PubMed1998

Effect of pindolol on onset of action of paroxetine in the treatment of major depression: intermediate analysis of a double-blind, placebo-controlled trial. Réseau de Recherche et d'Expérimentation Psychopharmacologique.

OBJECTIVE: The purpose of this study was to investigate the effect of pindolol to accelerate the onset of action of paroxetine in patients suffering from major depression. METHOD: Patients who met DSM-IV criteria for a nonpsychotic disorder, who had no previously treated episode of major depression episode, and who had a score of at least 18 on the 17-item Hamilton Depression Rating Scale were randomly assigned, for the first 21 days, to treatment with paroxetine (20 mg/day) and either pindolol (5 mg t.i.d.) or placebo. Patients were evaluated with the Hamilton depression scale, the Montgomery-Asberg Depression Rating Scale, and Global Clinical Impression (CGI) on days 0 (baseline), 5, 10, 15, 21, 25, 31, 60, 120, and 180. RESULTS: Intermediate analysis of the first month's results for the first 100 patients (pindolol, N=50; placebo, N=50) was performed. At day 10 there were more improved patients (defined as patients with a maximum score of 10 on the Hamilton depression scale) in the pindolol plus paroxetine group (N=24; 48%) than in the placebo plus paroxetine group (N=13; 26%). At day 5 there was no statistically significant difference, and at day 15 and thereafter, the differences between the two groups disappeared. Hamilton depression scale scores were significantly lower on days 5 and 10 for the pindolol plus paroxetine group (mean=15.7, SD=5.3, and mean=11.7, SD=6.4, respectively) than for the placebo plus paroxetine group (mean=19, SD=5.9, and mean=14.7, SD=6.8); this was also true for Montgomery-Asberg depression scale and CGI scores. CONCLUSIONS: The addition of pindolol to paroxetine treatment significantly accelerates the onset of therapeutic response in patients suffering from major depression. Nevertheless, the mechanism (pharmacodynamic or pharmacokinetic) of this beneficial effect remains unclear.

Adrenergic beta-Antagonists↗

PubMed1985

Significance of gonad and renal prostaglandin E2 in the antihypertensive effect of pindolol in spontaneously hypertensive rats.

The effect of gonadectomy on the antihypertensive action of pindolol in male spontaneously hypertensive rats (SHR) was investigated. And we also examined the relationship between the antihypertensive effect of this drug and the renal prostaglandin E2 (PGE2) level. In gonadectomized SHR, the reduction of blood pressure was not observed by the oral administration of pindolol, although the drug exhibited a marked antihypertensive activity in sham operated SHR. Urinary PGE2 in sham operated SHR was increased following the administration of pindolol, but not in gonadectomized SHR. Similar results were obtained in the experiments using Wistar rats. The PG synthesis inhibition induced by indomethacin suppressed the antihypertensive action of pindolol. Results in the present study suggest that renal PGs, particularly PGE2, are involved in the antihypertensive mechanism of pindolol, and that male gonad takes part in the regulation of the stimulation of the renal PGE2 producing system induced by pindolol.

Animals↗

PubMed1997

Pindolol augmentation of treatment-resistant depressed patients.

BACKGROUND: Recent uncontrolled reports describe a dramatic and rapid improvement of depressive symptoms in patients treated with the combination of pindolol and serotonin selective reuptake inhibitors or monoamine oxidase inhibitors. The present study attempts to replicate those findings. METHOD: Ten outpatients with current DSM-III-R major depressive disorder who had failed to obtain or maintain an appropriate response to an adequate trial of antidepressant drug were included in a randomized double-blind, placebo-controlled, crossover study. Subjects received pindolol 2.5 mg p.o. t.i.d. or placebo for 2 weeks in addition to their current antidepressant. Clinical monitoring, vital signs, and behavioral ratings were performed weekly for the duration of the study. RESULTS: Pindolol was well tolerated by all patients. None of the subjects experienced significant symptom worsening during the addition of either placebo or active drug. At the end of the 2-week trial, there was no statistically significant difference between pindolol augmentation and placebo. Two patients had a categorical response during placebo treatment. No categorical responses were observed during pindolol augmentation. CONCLUSION: This study failed to replicate the rapid and dramatic response to pindolol augmentation in treatment-resistant depressed patients.

Adrenergic beta-Antagonists↗

PubMed1977

Experiments with pindolol (Visken) in healthy volunteers.

Several aspects of beta-adrenoreceptor blockade in man can be investigated in healthy volunteers. Beta-adrenoreceptor blocking activity was investigated by measuring the influence on isoprenaline-induced tachycardia and on tachycardia due to exercise on the cycle ergometer. In these experiments pindolol was found to be 20 to 40 times more potent than propranolol. The partial agonist activity of pindolol is responsible for its small influence on heart rate under resting conditions, but probably also for its smaller effect on bronchial tone when compared with propranolol. A comparison of the duration of action of different drugs can be made by studying the effects on exercise-induced tachycardia. Two hours after oral administration, 5 mg of pindolol and 100 mg of propranolol were about equally active. The duration of action of pindolol, however, was clearly longer than that of propranolol. This should allow a single daily dose to be given to most patients for the treatment of hypertension. A comparison of beta-adrenoreceptor blocking activity after oral and intravenous administration provides information on the bioavailability of these drugs. In studies with pindolol the activities measured 2 hours after oral and 75 minutes after intravenous administration were about equal. This is in good agreement with the results of pharmacokinetic studies, which show almost complete absorption and a small first-pass effect of pindolol.

Biological Availability↗

PubMed1979

Therapeutic effects of pindolol and nifedipine in patients with stable angina pectoris and asymptomatic resting ischemia.

A single blind randomized parallel study designed to assess the anti-anginal efficacy of pindolol and nifedipine was carried out in 42 ambulatory coronary patients with stable angina pectoris. Drug efficacy was assessed in terms of (a) pain, (b) frequency of anginal episodes, (c) nitroglycerin consumption, (d) exercise tolerance and (e) ST-segment changes. The effect of these drugs on asymptomatic resting myocardial ischemia was also assessed by means of 24-h dynamic electrocardiography (DCG). All patients were checked at weekly intervals. At the end of a 4-wk placebo period, the patients were randomly assigned either to the pindolol or nifedipine group. The treatment lasted for 45 days. During the placebo period, ischemic ECG changes and symptoms of coronary insufficiency were detected in all patients. Furthermore, 12 out of 42 patients had asymptomatic myocardial ischemia at rest. One patient from each group was dropped because of tolerance. At the end of the 45-day study, pindolol and nifedipine were equi-effective on spontaneous and effort-related angina. There were, however, some differences: increased tolerance to exercise appeared earlier with pindolol: the pindolol group showed a slightly reduced while the nifedipine group showed a slightly increased heart rate. Furthermore, nifedipine reduced or eliminated asymptomatic myocardial ischemia in 6 out of 7 patients while only 1 out of 5 improved in the pindolol group.

Adult↗

PubMed1975

[Proceedings: The effect of beta receptor treatment with pindolol on the plasma renin activity and the left-ventricular dynamics in essential hypertension].

In 5 volunteers with essential hypertension (age between 32 and 48 years) plasma renin activity (PRA) was determined and right heart catheterization and femoral artery pressure measurements were carried out at rest and during isometric exercise by handgrip. Both investigations were repeated 88 to 98 days after continuous treatment with oral pindolol in increasing doses, the highest dose in all patients amounting to 45 mg/day. Following pindolol therapy arterial systolic cuff pressure decreased from 163 +/- 12 (1 SD) to 148 +/- 14 mm Hg (p less than 0,005). Diastolic cuff pressure decreased slightly but not significantly from 109 +/- 13 to 106 +/- 9 mm Hg. PRA varied in an inconsistent manner. Pulmonary capillary pressure (PCP), femoral artery mean pressure (FAM), cardiac output (CO) and systemic vascular resistance did not change significantly during treatment with pindolol. Stressing of the left ventricle by handgrip prior to and following pindolol elicited similar changes of heart rate, FAM, PCP, CO and stroke work. It is concluded (1) that pindolol produces only a small decrease in systolic cuff pressure, (2) that there is no correlation between changes in cuff pressure and PRA, and (3) that long-term treatment with pindolol is not accompanied by impairment of left ventricular function either at rest or during isometric exercise.

Adult↗

PubMed1987

Vasodilatory effects of carvedilol and pindolol.

The effects of three different nonselective beta-blockers on central and peripheral hemodynamics as well as on pulmonary function were compared in 13 healthy subjects (19-37 years). The subjects were given carvedilol 50 mg, pindolol 10 mg, propranolol 80 mg, and placebo orally twice daily for 1 week in a double-blind, crossover, randomized manner. Heart rate, blood pressure, arterial calf blood flow (venous occlusion strain gauge plethysmography), and pulmonary function (flow-volume spirometry) were measured at the first and at the last trial day. Heart rate and blood pressure were lower on carvedilol and propranolol than on pindolol and placebo; the maximal bradycardiac effect was 13 and 17 beats/min and hypotensive effect 9/10 mm Hg and 10/7 mm Hg on carvedilol and propranolol, respectively. Both carvedilol and pindolol increased arterial flow by about 40% (p less than 0.05 and p less than 0.01, respectively) and reduced peripheral resistance by about 34% (p less than 0.05 and p less than 0.01, respectively), the effect persisting after 1 week of treatment. None of the medications had any noteworthy effects on pulmonary function. Two subjects complained of tremor on pindolol. We conclude that carvedilol and pindolol possess distinct vasodilatory properties. Carvedilol had a stronger hypotensive effect than pindolol and was well tolerated.

Adrenergic beta-Antagonists↗

PubMed1989

[Clinical significance of intrinsic sympathomimetic activity of the beta blocker carteolol. II: Comparative studies of carteolol and pindolol in patients with bradycardia].

Completing previous studies in patients with sinus bradycardia (Med. Klin. 82 [1987], 647-650) we compared metoprolol with carteolol and pindolol, pindolol with carteolol, no treatment with carteolol (in two groups) in five series of the paired comparisons of Holter-ECG each. With change from metoprolol to carteolol or pindolol (dose ratio 10:1) lowest heart rate on Holter-ECG increased by 28 or 29% without change of exercise heart rate. Direct comparison of pindolol and carteolol revealed a very similar heart rate profile, indicating equipotent beta blockade and ISA. In patients with previous beta blocker induced bradycardia, carteolol did not change a normal resting heart rate off treatment. However, in patients with spontaneous sinus bradycardia carteolol increased lowest heart rate (+14%, due to overriding ISA) and lowered exercise heart rate (-15%, due to overriding beta blockade). A beta blocker induced sinus bradycardia consistently improved with change of treatment to carteolol and pindolol. With caution carteolol and pindolol may also be used despite spontaneous sinus bradycardia.

Adult↗

PubMed1989

Improvement in wall motion after pindolol: a mechanism for the preservation of left ventricular function in coronary artery disease.

1. In order to evaluate the mechanism by which beta blockers with intrinsic sympathomimetic activity preserve left ventricular systolic function at rest, 46 patients with coronary artery disease were studied by right and left heart catheterization and left ventriculography. Patients were studied using a double-blind, randomized protocol before and after a single intravenous dose of 3 mg propranolol (N = 22) or 0.5 mg pindolol (N = 24). 2. Mean right atrial pressure increased similarly after both drugs. Mean pulmonary artery pressure, left ventricular end-diastolic pressure, mean aortic pressure, and peripheral vascular resistance did not change significantly after either drug. Cardiac index (before: 3.0 +/- 0.7 (mean +/- SEM); after: 2.8 +/- 0.2 1 min-1 m-2) and heart rate (before: 78 +/- 15; after: 72 +/- 12 bpm) decreased only after propranolol administration. 3. Ejection fraction decreased only after propranolol (48 +/- 16 to 41 +/- 15%). Improvement in segmental wall motion abnormalities was noted (23 of 47 segments) only after pindolol. The total left ventricular wall motion score improved after pindolol and worsened after propranolol (P less than 0.05). In patients with impaired left ventricular function, pindolol administration resulted in improved resting ejection fraction. 4. Thus, the acute hemodynamic consequences of pindolol administration differ from those of propranolol owing to the preservation of left ventricular systolic function which seems to be related to the intrinsic sympathomimetic effect of pindolol on areas of reversible wall motion abnormality.

Adult↗

PubMed1978

A comparison between metoprolol and pindolol in the treatment of essential hypertension.

The antihypertensive effects on metoprolol and pindolol were compared in 50 patients with essential hypertension belonging to WHO stage 1 or 2. After four weeks of placebo treatment the patients were randomly allocated to treatment with metoprolol or pindolol. During the initial dose-titration period of six weeks the dose was individually adjusted, aiming at a diastolic blood pressure in the seated position less than 95 mm Hg. The maximum possible dosage for metoprolol was 50, 100 and 150 mg b.i.d. and for pindolol 5, 10 and 15 mg b.i.d. Thereafter followed a fixed-dose period of 20 weeks. Six patients did not complete the study. At the end of the study satisfactory blood pressure control, defined as a diastolic blood pressure in the seated position less than 95 mm Hg, was achieved in 15 of the 20 patients (75%) in the metroprolol group and in 13 out of 24 patients (54%) in the pindolol group. The average reduction in diastolic blood pressure was more pronounced with metoprolol than with pindolol, while no difference was found between the two beta-blockers with regard to the reduction of the systolic blood pressure. Generally, metoprolol and pindolol were both well tolerated by the patients.

Adrenergic beta-Antagonists↗

PubMed1985

[Comparative study of the central nervous system effect of the beta receptor blockaders pindolol and bisoprolol].

In a total of 36 volunteers with cardiac hyperreaction, investigations were carried out on the effect of bisoprolol (designated tradename: Concor), pindolol and placebo on central nervous functions with the aid of a reaction test, spiral aftereffect, tremor test and mood and sleep questionnaires. In the randomized double-blind study performed with 3 independent groups the volunteers received placebo, 2 X daily 10 mg of pindolol or 1 X daily 10 mg of bisoprolol for a period of 14 days. Bisoprolol is a new highly beta 1-selective adrenoceptor blocker with moderate lipophilia and without intrinsic sympathomimetic activity (ISA). When compared to placebo neither of the beta-adrenoceptor blockers induced any significant changes in mood, vigilance, tremor and reaction times. Moreover, under bisoprolol no negative effect on sleep quality or feeling refreshed after sleep was determined. Under pindolol, on the other hand, a significant impairment of sleep quality was observed after acute dosage and a decrease in feeling refreshed after sleep, continuing up to day 14 of treatment. It is presumed that, as bisoprolol and pindolol have comparable lipophilia, the different intensity with which the two preparations act on the central nervous system is connected with the ISA of pindolol. In the selected doses bisoprolol had a stronger effect on diastolic blood pressure and heart rate than pindolol and placebo.

Adult↗

PubMedDate not supplied

The influence of intrinsic sympathomimetic activity on regional left ventricular function; use of regional ejection fraction to demonstrate a beneficial action by pindolol over propranolol on hypokinetic segments.

In a previous report from our laboratory, visual assessment of wall motion in patients with coronary artery disease demonstrated no advantage for pindolol, a beta blocking agent with intrinsic sympathomimetic activity (ISA), over propranolol on impaired regional left ventricular (LV) function. In this study, we reanalyzed the radionuclide ventriculograms using a computer-assisted method of deriving regional ejection fraction. Use of normalized values allowed hypokinetic and normokinetic segments to be identified and examined separately. Pindolol (5-10 mg twice a day) was compared to propranolol (40-80 mg 4 times a day) in 23 patients using a randomized, crossover study design. Supine resting heart rate was reduced less (70 +/- 12 beats/min vs 63 +/- 10 beats/min, p less than 0.01) by pindolol; exercise heart rate was reduced equally by both agents. Derivation of normalized regional LV ejection fractions showed that 17 segments were hypokinetic at rest. Function of these segments increased (p less than 0.02) with pindolol. This improvement was not detected by visual assessment of regional wall motion. Thirty-seven segments were found to be hypokinetic during exercise and a significant (p less than 0.05) improvement in function occurred with pindolol and propranolol. In summary, derivation of normalized regional LV ejection fraction values allows the demonstration of significant improvement in resting LV function with pindolol, but not with propranolol in patients with regional dysfunction due to coronary artery disease. This advantage may provide a rationale for further evaluation of this agent in patients with more widespread ventricular dysfunction.

Angina Pectoris↗

PubMed1988

Discrepancy between central sympathoinhibitory action and peripheral hemodynamic effects of pindolol in anesthetized rats.

The present study was carried out to elucidate the relationship between changes in central sympathetic nerve activity and the peripheral hemodynamic effects of pindolol in anesthetized rats. Intravenous pindolol (0.1 mg/kg) produced a decrease in cardiac sympathetic nerve activity without a significant change in heart rate. Renal sympathetic nerve activity was also decreased by pindolol (0.1 and 0.5 mg/kg, i.v.) dose-dependently, but changes in mean arterial pressure were not dose-related. In addition, pindolol (0.1 and 0.5 mg/kg, i.v.) produced a dose-dependent reduction of preganglionic splanchnic nerve activity. These findings suggest that pindolol possesses a central sympathoinhibitory action, but there is a discrepancy between this central effect and peripheral cardiovascular effects of pindolol in rats.

Animals↗

PubMed1985

A possible role of antihypertensive polar renomedullary lipid (APRL) and prostaglandin E2 in the kidney in the antihypertensive action of pindolol.

The influence of the pretreatment with CV-3988, a specific antagonist of antihypertensive polar renomedullary lipid (APRL), and/or indomethacin on the antihypertensive effect of pindolol was examined in order to clarify a possible role of APRL and prostaglandin E2 (PGE2) in the kidney in the effect of pindolol in male spontaneously hypertensive rats (SHR). CV-3988 effectively attenuated the antihypertensive effect of pindolol, although pindolol still significantly lowered blood pressure following CV-3988 treatment. Besides, the pretreatment with CV-3988 showed no significant effect on an increased PGE2 level and a decreased volume of urine after pindolol treatment. The antihypertensive effect of pindolol disappeared after the CV-3988 treatment in combination with indomethacin.

Animals↗