Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pindolol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed2002

[Effect of (+/-)-pindolol on the central 5-HT1A receptor by the use of in vivo microdialysis and hippocampal slice preparations].

Although it is suggested that (+/-)-pindolol, a beta-adrenergic/5-HT1A receptor antagonist, may enhance the efficacy of selective serotonin reuptake inhibitors (SSRI), the results of double-blind studies are contradictory and recent animal studies suggest that (+/-)-pindolol may act as a partial agonist to the 5-HT1A receptor. In this study we have investigated the effect of (+/-)-pindolol on both pre- and postsynaptic 5-HT1A receptors using in vivo microdialysis and hippocampal slice preparations. (+/-)-pindolol and flesinoxan, a 5-HT1A receptor full agonist, significantly decreased the extracellular levels of 5-HT in the raphe and prefrontal cortex. The 5-HT and other 5-HT1A receptor agonists, flesinoxan and 8-hydroxy-2- (di-n-propylamino)tetralon (8-OH-DPAT), significantly decreased the population excitatory postsynaptic potential (EPSP) in the CA3-CA1 excitatory synapse in a dose-dependent manner. The effect of 5-HT and other 5-HT1A receptor agonists accompanied the increase in paired-pulse facilitation (ppf) induced by short-interval two stimuli and were reversed by the coadministration of the 5-HT1A receptor agonist, NAN-190, but not by (+/-)-pindolol. (+/-)-pindolol also suppressed the EPSP, but this effect was not reversed by NAN-190. These results suggest that (+/-)-pindolol acts as a partial agonist to the somatodendritic 5-HT1A receptor in the raphe, whereas it may have no action on the postsynaptic 5-HT1A receptor in the hippocampus.

Animals↗
PubMed1986

Effects of pindolol and propranolol on beta adrenergic receptors on human lymphocytes.

The cardiovascular supersensitivity observed after discontinuation of administration of beta adrenergic receptor antagonists may be explained by an increase in the density of beta adrenergic receptors. Thus, a change in the density of receptors has been observed in human lymphocytes after administration of propranolol (Aarons et al., 1980). The effects of pindolol, a beta adrenergic receptor antagonist with intrinsic sympathomimetic activity, were compared with those of propranolol or placebo. Pindolol (10 mg q.i.d.), propranolol (40 mg q.i.d.) or placebo were administered to 12 subjects for 8 days. The density of beta adrenergic receptors was determined by Scatchard analysis of the specific binding of [125I]iodopindolol on membranes prepared from human lymphocytes. Administration of pindolol resulted in a 30 to 50% decrease in the density of beta adrenergic receptors. This decrease was apparent within 1 day of beginning pindolol administration and it persisted for at least 8 days after discontinuation of drug administration. The reversibility of the decrease in receptors observed after pindolol administration was studied in 27 subjects given propranolol, pindolol or placebo for 4 days in a double-blind cross-over trial. Propranolol consistently induced a small increase in the density of beta adrenergic receptors. The density of receptors returned to predrug values within 2 days after discontinuation of propranolol administration. Pindolol induced a 30 to 50% decrease in the density of receptors which, as observed previously, persisted for at least 10 days after discontinuation of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of pindolol administration on serum levels of thioridazine, haloperidol, phenytoin, and phenobarbital.

Twenty-six male patients with intermittent explosive disorder secondary to organic brain disease were studied. Each had been treated with long-term administration of thioridazine, haloperidol, phenytoin, and/or phenobarbital, either singly or in combination. The effect of adding increasing doses of pindolol--a beta-adrenergic blocking agent previously demonstrated to be effective in the treatment of intermittent explosive disorder--on serum levels of each long-term medication was determined. Moderate, dose-related increases in serum levels of thioridazine and two of its metabolites were found when pindolol was added. Conversely, higher-than-expected serum pindolol levels occurred in patients receiving thioridazine. No serum level increases were found for haloperidol, phenytoin, or phenobarbital when pindolol was added to each of these drugs individually, but serum phenytoin levels did rise in two patients receiving all three drugs simultaneously when pindolol was added. Three treatment failures with pindolol occurred in association with low serum pindolol levels.

Adult↗
PubMed1983

A comparative study on the effects of pindolol and propranolol on systemic and cardiac haemodynamics in hypertensive patients.

Eight out-patients with essential hypertension participated in a comparative, placebo-controlled study with a cross-over design. Pindolol and propranolol were administered orally in doses of 20.0 +/- 3.13 mg/d (mean +/- SEM) and 125.0 +/- 19.17 mg/d respectively. Pindolol reduced mean blood pressure by 11.9 mmHg; pre-ejection period index by 8.1 msec; total peripheral resistance by 3.1 mmHg min/L; and limb vascular resistance by 3.28 mmHg min 100 g/ml. Heart rate, cardiac output, plasma renin activity and urinary norepinephrine excretion rate were not altered by pindolol. Propranolol reduced mean blood pressure by 14.0 mmHg; heart rate by 9.1 beats/min; cardiac output by 0.57 L/min; limb blood flow by 1.06 ml/100 g.min; and plasma renin activity by 1.44 ng/ml/h; and increased pre-ejection period index by 8.7 msec. Total peripheral resistance, limb vascular resistance and urinary norepinephrine excretion rate were not altered by propranolol. It was concluded that: (1) the drugs, pindolol and propranolol, are equally effective as antihypertensive agents; (2) heart function and plasma renin activity are decreased by propranolol and unaltered by pindolol; (3) total peripheral resistance is decreased by pindolol and unaltered by propranolol; and (4) these findings may be explained by the intrinsic sympathomimetic activity exhibited by pindolol only.

Adult↗
PubMed1984

Long-term effect of pindolol on plasma lipids, apoproteins A, blood glucose, and serum insulin levels.

The present investigation was designed to study the effect of 12-month therapy with pindolol on serum lipids, apoproteins A, insulin, and blood glucose levels. The concentration of serum HDL-cholesterol was increased (P less than 0.05) during the 1st month of therapy. The ratio of HDL-cholesterol to total cholesterol increased slightly during therapy, but this increase was significant (P less than 0.05) only after 6 months. The total serum cholesterol level was lower (p less than 0.05) after 6 months than after 1 month of therapy. The concentrations of LDL-cholesterol showed a slight tendency to decrease during treatment. The concentrations of serum free fatty acids and triglycerides remained about constant during treatment. No significant changes in the concentrations of apolipoproteins A-I and A-II were found during the therapy with pindolol. Fasting blood glucose concentrations did not show a significant change after 12-month treatment with pindolol. During the oral glucose tolerance test, blood glucose values were raised after pindolol therapy slightly at 60 and significantly at 120 min. No significant changes in the levels of serum insulin during the glucose tolerance test were found after treatment with pindolol. Pindolol may induce glucose intolerance without impairment in insulin release. A comparison of the results of this study with previous reports on other beta blockers suggests that pindolol might have fewer untoward effects on lipid metabolism than other beta blockers.

Apolipoproteins↗
PubMed1984

Effect of pindolol on potassium homeostasis in patients with essential hypertension.

A study of the effects of pindolol on potassium homeostasis was undertaken in 25 patients (19 women, 6 men) with essential hypertension. The patients were maintained on their usual diet and were withdrawn from antihypertensive therapy for three weeks before the study began. They were then randomly assigned to one of three treatment groups: (a) pindolol, 15 mg daily; (b) hydrochlorothiazide, 50 mg daily; and (c) both drugs combined. Total body potassium (TBK), urine aldosterone excretion, and plasma renin activity (PRA) were measured after eight weeks of therapy and compared with pretreatment values. Mean PRA remained unchanged in patients taking only pindolol or the drug combination, but it rose significantly in patients taking only hydrochlorothiazide. Mean urine aldosterone concentrations fell in patients taking only pindolol, rose in those taking only hydrochlorothiazide, and remained unchanged in those taking the combination. Mean TBK concentrations rose significantly in patients taking only pindolol or the combination, and fell significantly in those taking only hydrochlorothiazide. The rise in TBK concentrations with the combination clearly suggests that pindolol offsets the potassium wastage induced by diuretics, though probably by a mechanism outside the renin-aldosterone system. Because of this rise, it may be possible to eliminate potassium supplementation in patients taking the combination pindolol and hydrochlorothiazide.

Adult↗
PubMed1976

Twice-daily pindolol and alprenolol in essential hypertension of moderate severity.

A double-blind cross-over comparison of the antihypertensive actions of alprenolol and pindolol in equipotent doses was carried out in 22 patients with moderately severe essential hypertension. No other drugs were allowed. Ten patients were in WHO grade I, and 12 in grade II. The average initial pressures, similar after both the first and second 4-week placebo periods, were 175/116 mm Hg standing and 175/109 mm Hg supine. These pressures were decreased significantly by each beta-blocking drug, and about equally in both positions. An average reduction, using both 2-month treatment periods, was -13/-7 mm Hg with alprenolol, and with pindolol it was -23/-13 mm Hg. Both systolic and diastolic normotension (less than 160/100) in the supine position occurred in 45% of the patients when treated with alprenolol and in 64% with pindolol. With diastolic normotension alone the figures were 59% and 82% respectively. Rather low daily doses of 400 mg alprenolol and 20 mg pindolol were effective; increasing the doses to the average final levels of 533 mg alprenolol and 25 mg pindolol resulted in just negligible further pressure reductions. There were no serious side effects or complete resistance. Pindolol reduced the resting heart rate significantly in spite of its intrinsic sympathomimetic activity. Two aspects emerging from this study have clear practical implications. The twice-daily dosage, used here purposefully, of both alprenolol and of pindolol reduces effectively blood pressure, and increases patient convenience. Heat failure was not induced even in those 12 patients with cardiac involvement, including 5 with clear-cut radiological left ventricular enlargement.

Administration, Oral↗
PubMed2005

Pindolol augmentation of selective serotonin reuptake inhibitors: accounting for the variability of results of placebo-controlled double-blind studies in patients with major depression.

Co-administration of pindolol with SSRIs in patients with depression has been suggested as a way to both hasten and augment antidepressant response. Clinical trials have examined the efficacy of this treatment regime and conflicting results have been reported. The present review briefly presents the results of placebo-controlled double-blind trials of pindolol augmentation of SSRIs in patients with major depression, and focuses on factors that may account for the variability of findings. Additionally, a profile of the subset of patients who may most benefit from pindolol augmentation is outlined. Methodological factors such as qualitative differences in definitions of antidepressant response, the timing of pindolol administration and heterogeneous clinical characteristics of patient samples may contribute to the variability in the results of clinical trials to date. Similarly, individual differences in neuropathology, neurophysiology and genotype may also account for some of the inconsistencies in the findings. Finally, the results of recent neuroimaging studies suggest that the 2.5 mg t.i.d. dose of pindolol that has been used in all but one of these investigations may be suboptimal for achieving reliable and significant occupancy of 5-HT1A autoreceptors and may explain the contradictory nature of the results of investigations of pindolol augmentation.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Pindolol: a review of its pharmacology, pharmacokinetics, clinical uses, and adverse effects.

Pindolol is a new noncardioselective beta adrenergic blocking agent with intrinsic sympathomimetic activity. In the treatment of mild to moderate hypertension, pindolol provides effective control of blood pressure in a large majority of patients when administered alone or, more commonly, when combined with a thiazide diuretic. Pindolol is approximately as effective as propranolol in the therapy of hypertension, but in some crossover trials central nervous system side effects were more frequent with pindolol. A "ceiling effect" may be observed as dosages are titrated upward above approximately 20 to 30 mg per day, such that further blood pressure reductions may not be achievable. Some patients will exhibit a paradoxical increase in blood pressure with an increase in dosage. In patients who respond to modest doses of pindolol, twice or even once daily dosing is often adequate. This prolonged duration of hypotensive activity, while not suggested by the kinetics of this or similar drugs, is probably common to most beta blockers. Investigations in small numbers of patients with angina pectoris have reported variable but generally beneficial results with pindolol.

Adrenergic beta-Antagonists↗
PubMed1984

Chronotropic effects of pindolol. Relation between ventricular effects and control resting ventricular rate values in conscious dogs with chronic A-V block.

The chronotropic effects of pindolol were studied in the conscious dog with chronic A-V block. Pindolol significantly increased atrial rate, probably through both its strong intrinsic sympathomimetic activity and reflex withdrawal of atrial vagal tone in response to its hypotensive effect. Pindolol did not alter ventricular rate overall. However, in individual dogs, pindolol caused ventricular chronotropic effects that were inversely related to resting ventricular rate: it increased ventricular rate when the resting ventricular rate was low and reduced it when it was high. In view of the fact that pindolol is a beta-adrenoceptor antagonist endowed with a strong intrinsic sympathomimetic activity, this finding contributes to a better understanding of how pindolol affects heart rate.

Animals↗
PubMed1982

Simplified antihypertensive therapy with pindolol retard.

36 out of 52 patients with essential hypertension, whose blood pressure was not normalized with pindolol 15 mg per day, were treated with 30 mg per day for four to six weeks. Pindolol was administered in random order, either as 15 mg twice daily or as one 30 mg retard tablet once daily. Blood pressure was lowered from mean pretreatment levels of 174/111 mmHg to 149/98 mmHg by 15 mg b.d., and to 145/97 mmHg by 30 mg retard. In five patients diurnal variations in blood pressure and plasma pindolol levels were determined. At all times during the day blood pressure was at least well controlled by 30 mg retard as by 15 mg b.d. Plasma concentration maxima were similar with both forms, but a higher concentration was maintained for a longer time after the retard tablet. Pindolol 30 mg was well tolerated and the incidence of side effects was lower than during treatment with 15 mg b.d. Thus, patients requiring high doses of pindolol for control of hypertension can safely and conveniently be treated with a single tablet of 30 mg pindolol retard.

Blood Pressure↗
PubMed1985

Atenolol versus pindolol: side-effects in hypertension.

This randomized crossover out-patient study was designed to compare the antihypertensive effects of atenolol and pindolol. After a wash-out period of two weeks in pretreated cases, 107 patients with essential hypertension were given either atenolol 100 mg once-daily or pindolol 20 mg slow release (SR) once-daily. Both atenolol and pindolol lowered blood pressure over the 24 week period. The diastolic blood pressure reduction was significantly greater (p less than 0.01) with atenolol than with pindolol. Before beta-blocker therapy, many patients had already experienced side-effects such as fatigue, sleep disturbances and dreams. This probably relates to the high sensitivity of the analogue scale used to assess side-effects, and to the high incidence of such symptoms in untreated patients. As the study progressed there was a reduction in the frequency of fatigue (p less than 0.03) and dreams (p less than 0.05) in both groups, whereas sleep disturbances significantly increased under pindolol (p less than 0.05) but decreased under atenolol (p less than 0.05). The only important side-effect difference between the two beta-blockers was the higher incidence of sleep disturbances with pindolol which may be due to the higher lipophilicity of this beta-blocker.

Adolescent↗
PubMed1982

Elimination of pindolol in liver disease.

The elimination of pindolol was studied in 32 patients suffering from various liver diseases, mainly acute hepatitis and hepatic cirrhosis. The total body clearance of antipyrine was measured simultaneously as a parameter of liver microsomal enzyme activity. The doses given were antipyrine 1000 mg orally and pindolol 3 mg i.v. Plasma samples were taken and urine was collected for up to 72 h for the measurement of drug concentrations. In addition, conventional biochemical laboratory tests were done. The total body clearance of antipyrine was compared with the pharmacokinetic parameters calculated for pindolol, and the results of the biochemical tests. No correlation was found between antipyrine clearance and the routine biochemical parameters in liver disease or with the total body clearance of pindolol. A significant correlation was seen with the nonrenal clearance of pindolol taken as representing its major metabolic degradation. Higher correlation coefficients were observed when two subgroups of patients with acute hepatitis and hepatic cirrhosis were separated. In some patients suffering from hepatic cirrhosis a higher urinary excretion of unchanged pindolol was observed as liver function become decompensated, a finding due to an unknown mechanism but based on intact renal function. In patients with acute hepatitis a much higher nonrenal clearance was found than in many other patients, which might be based on increased liver blood flow.

Adolescent↗
PubMed1979

beta-Adrenoceptor blocking effects and pharmacokinetics of pindolol. A study in hypertensive Africans.

The beta-adrenoceptor blocking effects of pindolol were compared with those of a placebo in a double-blind trial in twelve hypertensive Africans. Heart rate and arterial blood pressure were measured at rest and immediately after exercise, before and at intervals up to 8 h after oral administration of the drugs. Plasma levels of pindolol were also determined. Pindolol reduced systolic blood pressure and antagonised exercised-induced tachycardia. The mean time to peak level of pindolol was 1.9 h and the mean half-life was 4.2 h. Comparison of plasma levels of pindolol and beta-adrenoceptor blocking activity showed good correlation between them. It is concluded that the pharmacokinetics and beta-blocking effects of pindolol in Africans are not dissimilar from published data for other races.

Adrenergic beta-Antagonists↗
PubMed1980

Influence of propranolol and pindolol on the haemodynamic effects of papaverine, isoprenaline and noradrenaline in hypertensive patients.

The influence of two beta-adrenoceptor antagonists, propranolol and pindolol, on the haemodynamic effects of papaverine, isoprenaline and noradrenaline was investigated in 9 male patients with first degree essential hypertension. Propranolol and pindolol were given according to a doubleblind, crossover scheme. Heart rate and blood pressure were measured before and after each treatment. Propranolol 670 microgram/kg i.v. reduced the supine and standing systolic blood pressures by 2.3% and 1.6%, respectively. Similarly, the intravenous administration of pindolol 35 microgram/kg reduced supine and standing systolic blood pressure by 5.5% and 8.3% respectively (clinically insignificant). Neither drug affected diastolic blood pressure. Following propranolol, there were moderate reduction in supine and standing heart rates, respectively by 24% and 20% (p < 0.001). Similarly, but to a lesser extent, pindolol reduced supine and standing heart rate by 12% and 17% (p < 0.001). The effects of papaverine, which, at 1.5 mg/kg i.v. reduced systolic blood pressure by 5-10% and increased heart rate by 8-15%, were not significantly influenced by the beta-blockers. The blood pressure and heart rate responses to isoprenaline, on the other hand, were attenuated or inhibited by both beta-blockers. While the beta-blockers inhibited the beta-adrenoceptor component of noradrenaline, the pressor component of noradrenaline, which is mediated through the alpha-adrenoceptors, was not influenced by propranolol, but was inhibited after pindolol. It is concluded that pindolol differs qualitatively from propranolol in that it inhibited both the alpha and beta-adrenoceptor effects of noradrenaline.

Adult↗
PubMed1978

Activity and duration of action of pindolol and alprenolol compared in healthy volunteers.

An improvement in the prognosis of myocardial infarction has been reported after long term treatment with alprenolol 200 mg twice daily. Therefore, an experiment was carried out to find the dose of pindolol given once daily which would show cardiac beta-adrenoceptor blockade at least equipotent to that obtained during treatment with alprenolol 200 mg twice daily. Cardiac beta-adrenoceptor blocking activity and its time course during treatment with pindolol (15 mg and 20 mg given once daily) and alprenolol (200 mg given 12-hourly) for three days were compared in 6 healthy volunteers. The reduction in exercise-induced tachycardia as a measure of cariac beta-adrenoceptor blockade was significantly greater after pindolol 15 mg and 20 mg than after alprenolol 200 mg. On the morning of the fourth day, i.e. 24 h after the last dose of pindolol and only 12 h after the last dose of alprenolol, the effects of pindolol at both dose levels were slightly greater than those of alprenolol. This difference was not statistically significant. It can be concluded that pindolol 15 mg once daily produces a cardiac beta-adrenoceptor blockade at least equipotent to that of alprenolol 200 mg given 12-hourly.

Adult↗
PubMed1986

Beta-blocking effect and pharmacokinetics of pindolol in young and elderly hypertensive patients.

The pharmacokinetics and beta-blocking effect of pindolol has been compared in 20 patients with essential hypertension (WHO Stage I), 10 below 25 years of age and 10 older than 60 years. Each patient received pindolol 10 mg p.o. once a day for 5 days. The area under the curve (AUC) of pindolol was larger in the old than in the young patients both on the first (p less than 0.05) and the fifth (p less than 0.01) days. The AUC of pindolol was 14% higher on the fifth day compared to the first day in the elderly group, indicating minor accumulation at steady-state. There was no change in AUC in the young patients. Endogenous creatinine clearance was lower in the old (80 +/- 9 ml/min) than in the young patients (150 +/- 45 ml/min). The beta-blocking effect did not differ between the groups at 2 h after administration of pindolol on Days 1 or 5. However, 24 h after the first and fifth doses approximately 60% of the beta-blockade persisted in the old group whereas 17 and 19% of the beta-blockade, respectively, persisted in the young group; the difference between the groups was statistically significant (p less than 0.01). The most probable explanation for the more sustained beta-blocking effect in the elderly is the physiologically decrease in renal function, which results in a more sustained plasma level of pindolol in those patients.

Adrenergic beta-Antagonists↗
PubMed2001

Pindolol antagonises G-protein activation at both pre- and postsynaptic serotonin 5-HT1A receptors: a.

The arylalkylamine, pindolol, may potentiate the clinical actions of antidepressant agents. Although it is thought to act via blockade of 5-HT1A autoreceptors, its efficacy at these sites remains controversial. Herein, we evaluated the actions of pindolol at 5-HT1A autoreceptors and specific populations of postsynaptic 5-HT1A receptors employing [35S]GTPgammaS autoradiography, a measure of receptor-mediated G-protein activation. Both 8-OH-DPAT (1 microM) and 5-HT (10 microM) elicited a pronounced increase in [35S]GTPyS binding in the dorsal raphe nucleus, which contains serotonergic cell bodies bearing 5-HT1A autoreceptors. Pindolol abolished their actions. In the dentate gyrus, lateral septum and entorhinal cortex, structures enriched in postsynaptic 5-HT1A receptors, 8-OH-DPAT (1 microM) and 5-HT (10 microM) also elicited a marked increase in [35S]GTPgammaS binding which was likewise blocked by pindolol. The antagonism of 5-HT-induced [35S]GTPgammaS labelling in the dentate gyrus was shown to be concentration-dependent, yielding a pIC50 of 5.82. Pindolol did not, itself, affect [35S]GTPgammaS binding in any brain region examined. In conclusion, these data suggest that, as characterised by [35S]GTPgammaS autoradiography, and compared with 5-HT and 8-OH-DPAT, pindolol possesses low efficacy at both pre- and postsynaptic 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗