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PubMed2003

EEG effects of buspirone and pindolol: a method of examining 5-HT1A receptor function in humans.

RATIONALE: An involvement of 5-HT(1A) receptors is postulated in the pathophysiology of affective disorders and mechanism of action of antidepressants. Methods for studying their functional integrity in humans are, however, limited. Preliminary data suggests that activation of somatodendritic 5-HT(1A) receptors cause a negative shift in the EEG frequency spectrum. Animal research suggests that pindolol is an agonist at these receptors but an antagonist at postsynaptic 5-HT(1A) receptors. OBJECTIVE: We postulated that while pindolol would antagonise known postsynaptic mediated neuroendocrine responses to the 5-HT(1A) agonist buspirone, both drugs would have a similar effect on the EEG frequency spectrum. METHODS: Fourteen healthy men were administered placebo or pindolol (20 mg orally) 90 min before placebo or buspirone (30 mg orally) in a double blind cross-over study. Plasma prolactin and growth hormone were assayed and EEGs recorded before and after drug administration. RESULTS: A significant negative shift in the EEG frequency spectrum was found for both buspirone and pindolol, with the combination producing a similar effect to each drug alone. In contrast, the neuroendocrine response to buspirone was significantly attenuated by pindolol. CONCLUSIONS: The data obtained are consistent with the EEG effects of buspirone and pindolol being mediated by somatodendritic 5-HT(1A) receptors, in contrast to the neuroendocrine response, which is known to be mediated by postsynaptic receptors. The development of this novel method of assessing somatodendritic 5-HT(1A) receptors in humans is a potentially important advance which may allow the testing of hypotheses of its involvement in depression and response to antidepressants.

Adolescent↗
PubMed1998

Pindolol does not act only on 5-HT1A receptors in augmenting antidepressant activity in the mouse forced swimming test.

The present study was undertaken to identify the receptor subtypes involved in (+/-) pindolol's ability to enhance the effects of antidepressant drugs in the mouse forced swimming test. Interaction studies were performed with S 15535 (presynaptic 5-HT1A receptor agonist) and methiothepin (5-HT1B autoreceptor antagonist) in an attempt to attenuate or potentiate antidepressant-like activity. (+/-) Pindolol was tested in combination with selective agonists and antagonists at 5-HT1, 5-HT2 and 5-HT3 receptor subtypes. Pretreatment with S 15535 and methiothepin attenuated the activity of paroxetine, fluvoxamine and citalopram (32 mg/kg, i.p.; P < 0.01). (+/-) Pindolol (32 mg/kg, i.p.) induced significant anti-immobility effects when tested in combination with 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridyl)-1H-indole (RU 24969) (1 mg/kg, i.p.; P < 0.05), 1-(2-methoxyphenyl)-4-[-(2-phthalimido) butyl]piperazine) (NAN 190) (0.5 mg/kg; P < 0.05) and ondansetron (0.00001 mg/kg, i.p.; P < 0.01). Pretreatment with NAN 190 (0.5 mg/kg, i.p.) potentiated the effects of RU 24969 (1 mg/kg, i.p.; P < 0.05) and (+/-) pindolol (32 mg/kg, i.p.; P < 0.05) in the forced swimming test, as did ondansetron (0.00001 mg/kg, i.p.). Significant additive effects were induced when RU 24969 (1 mg/kg, i.p.) was tested in combination with NAN 190 (0.5 mg/kg, i.p.; P < 0.05), (+/-) pindolol (32 mg/kg, i.p.; P < 0.05) and ondansetron (0.0000 mg/kg, i.p.; P < 0.05). 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (1 mg/kg, i.p.) or ketanserin (8 mg/kg, i.p.) did not induce significant antidepressant-like effects with any of the agonists/antagonists tested. The results of the present study suggest that pindolol is acting at presynaptic 5-HT1B serotonergic receptors, in addition to the 5-HT1A subtype, in augmenting the activity of antidepressants in the mouse forced swimming test.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of pindolol and methyldopa on blood pressure and plasma norepinephrine.

Thirty patients with essential hypertension (supine diastolic blood pressure 100 to 115 mm Hg) were treated in a randomized, double-blind study with either pindolol (mean dose 28 +/- 5 mg twice a day) or methyldopa (673 +/- 158 mg three times a day) for 12 weeks after a 3-week, single-blind placebo period. In 17 pindolol-treated patients mean supine blood pressure was 163 +/- 3/106 +/- 1 during the placebo period and 155 +/- 3/99 +/- 2 mm Hg (p less than 0.01) during the high-dose period. In 13 patients treated with methyldopa mean supine blood pressure fell from 160 +/- 4/104 +/- 1 to 156 +/- 5/97 +/- 2 mm Hg. Mean standing heart rate was reduced during pindolol therapy from 84 +/- 2 to 79 +/- 2 bpm (p less than 0.05) but was unchanged during methyldopa treatment. Mean supine pretreatment plasma norepinephrine fell from 379 +/- 40 to 337 +/- 33 pg/ml in patients on pindolol therapy and from 448 +/- 76 to 223 +/- 39 pg/ml (p less than 0.02) in the methyldopa-treated group. Although norepinephrine generally decreased in pindolol responders and not in nonresponders, changes in supine diastolic blood pressure and supine plasma norepinephrine did not correlate. In contrast, norepinephrine declined consistently in methyldopa-treated patients regardless of the blood pressure response; changes in diastolic blood pressure and norepinephrine correlated (r = 0.59; p less than 0.05). The results suggest that suppression of sympathetic nervous system activity may play a role in the hypotensive effect of both pindolol and methyldopa.

Blood Pressure↗
PubMed1982

Pindolol and systolic time intervals in patients with hypertension.

Two studies of systolic time intervals (STIs) in patients with mild to moderate hypertension (HBP) revealed that no mean change in systolic intervals occurred with pindolol therapy, although some patients had significant alterations in their STIs. Pindolol responders with normal pretreatment preejection period to left ventricular ejection time (PEP/LVET) ratios had a significant increase in this ratio following pindolol therapy, whereas those with abnormal pretreatment PEP/LVET ratios had improvement in this ratio on administration of the drug. Patients on propranolol showed no change in PEP/LVET ratio. Propranolol administration slowed heart rate and lengthened Q-S2, S1-S2, and LVET, however, without altering the Q-S2 and LVET index, indicating that the changes were caused by the effect of propranolol on the heart rate alone. Chlorthalidone in high doses significantly reduced the Q-S2 index and the S1-S2 index, indicating that these changes were not caused by alteration of the heart rate. The second study suggests that STIs may provide a predictive clue for clinical response to pindolol. Patients with normal cardiac function (group I) are more likely to respond to pindolol than are those with abnormal cardiac function (group II). Directionally opposite changes in STIs in the two subgroups suggest different mechanisms for changing cardiac function. Pindolol's dual role as a beta-blocking agent with intrinsic sympathomimetic activity is proposed as a possible explanation, beta-blocking effects predominating in group I and sympathomimetic activity balancing the beta effect in group II.

Adult↗
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↗
PubMed1988

Comparison of the effects of pindolol and atenolol on hemodynamic function in systemic hypertension.

A randomized double-blind study was performed on a group of mild hypertensive patients (WHO class I) to compare the hemodynamic effects of pindolol and atenolol. Blood pressure (BP) was monitored with a mercury gauge sphygmomanometer, while cardiac function and peripheral arterial flows were measured by the noninvasive technique of bioelectric impedance. After a 2-week washout period, patients with a diastolic BP greater than 95 mm Hg but less than 114 mm Hg were randomized into the pindolol (29 patients) or atenolol (28) treatment groups. Patients were treated with 1 of the 2 drugs in an incremental fashion for 12 weeks. Cardiovascular function was measured after the washout period and at the end of the 12-week treatment period. Baseline hemodynamics were similar in both groups. The 2 drugs were equally effective in lowering both systolic and diastolic BP. Hemodynamically, pindolol lowered BP by decreasing total peripheral resistance (-406 +/- 145 dynes.s.cm-5) while atenolol decreased cardiac index (-0.2 +/- 0.1 liters/min/m2) associated with a decrease in heart rate (-12 +/- 2 beats/min). Regarding peripheral vascular beds, pindolol lowered arm vascular resistance (-198 +/- 72 mm Hg/liter/min) and leg vascular resistance (-73 +/- 25 mm Hg/liter/min), especially when subjects who did not respond to pindolol were excluded from the analysis. Both arm (5.5 +/- 5.4% increase above baseline) and leg (1.2 +/- 4.4% increase above baseline) arterial flow indexes were maintained with pindolol. Conversely, atenolol decreased the arm arterial flow index (-9,8 +/- 5.6% decrease below baseline), but not significantly and with no change in resistance (+54 +/- 62 mm Hg/liter/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Catecholaminergic and opioidergic mechanisms involved in the hypotensive response of pindolol.

The present study evaluated the involvement of opioidergic and catecholaminergic mechanisms in the hypotensive action of pindolol. Pindolol (1 mg/kg i.a.) was administered to unanesthetized spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats instrumented for direct arterial pressure monitoring. Peripheral administration of pindolol produced a significant decrease in blood pressure in both SHR and WKY rats with SHR animals having a greater response. Heart rate was reduced in SHR; however, a tachycardia was observed in WKY rats. Pretreatment with naloxone (100 micrograms/kg i.a.) 10 min prior to pindolol administration prevented the hypotensive response. Similar pretreatment with yohimbine, an alpha 2-receptor antagonist, also prevented the pindolol-induced hypotensive response in both SHR and WKY rats. Neither naloxone nor yohimbine alone significantly affected blood pressure or heart rate. These results suggest that opioidergic and catecholaminergic mechanisms are involved in the hypotensive action of pindolol.

Animals↗
PubMed1994

Stereoselective antagonism by the pindolol enantiomers of 8-OH-DPAT-induced changes of sleep and wakefulness.

The effects of 5-HT1A receptor agonist 8-OH-DPAT were compared with those of the mixed beta-adrenoceptor and 5-HT1A receptor antagonist (-)pindolol, and the selective beta-adrenoceptor antagonist betaxolol in rats implanted for chronic sleep recordings, 8-OH-DPAT (0.375 mg/kg) significantly increased wakefulness and decreased slow wave sleep (SWS) and REM sleep (REMS). At 2.0-4.0 mg/kg (-)pindolol reduced REMS. Betaxolol in doses of 1.0 and 2.0 mg/kg did not significantly modify sleep variables. Pretreatment with (-)pindolol (2.0-4.0 mg/kg) reversed the effect of 8-OH-DPAT on waking and SWS, while (+)pindolol (4.0 mg/kg) and betaxolol (2.0 mg/kg) were ineffective in this respect. The stereoselective antagonism by the pindolol enantiomers supports the proposal that 8-OH-DPAT-induced increase of waking and decrease of SWS depends on the activation of 5-HT1A receptors. The absence of antagonism by betaxolol tends to indicate that prevention by (-)pindolol of waking increase did not involve beta-adrenoceptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

(-)-pindolol and (+/-)-tertatolol affect rat hippocampal 5-HT levels through mechanisms involving not only 5-HT1A, but also 5-HT1B receptors.

The present work examined, using in vivo microdialysis, the effects of 0.16-10 mg/kg of the beta-adrenoceptor antagonists, (-)-pindolol and (+/-)-tertatolol, which have additional 5-HT1A receptor antagonist properties, on extracellular 5-HT levels in the ventral hippocampus of chloral hydrate-anaesthetized rats. These effects were compared with those observed when (-)-pindolol and (+/-)-tertatolol were given together with the 5-HT1A agonist 8-OH-DPAT (0.31 mg/kg i.p.). When given alone, (-)-pindolol and (+/-)-tertatolol increased 5-HT levels not only after systemic administration (at 2.5 and 10 mg/kg s.c.), but also when perfused locally through the dialysis probe (at a concentration of 10 microM). At doses equal to or lower than those that increased 5-HT when given alone, (-)-pindolol and (+/-)-tertatolol inhibited the decrease of extracellular 5-HT levels induced by 8-OH-DPAT. At higher doses, however, (-)-pindolol and (+/-)-tertatolol were less able to reverse these effects of 8-OD-DPAT. The selective beta 1-adrenoceptor antagonist, (+/-)-betaxolol, did not alter 5-HT levels, either when given alone or when given together with 8-OD-DPAT. Although the antagonism of the 8-OH-DPAT-induced decrease of 5-HT levels by (-)-pindolol and (+/-)-tertatolol is likely to be related to their 5-HT1A antagonist properties, their ability to increase extracellular 5-HT levels when given alone may involve interactions with 5-HT1B receptors at hippocampal 5-HT terminals.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1983

Effects of pindolol on vascular smooth muscle.

Pindolol is a non-selective beta-adrenoceptor blocking agent with relatively marked intrinsic sympathomimetic activity. Stimulant effects in isolated, perfused mesenteric vessels (beta 2) equal those of isoprenaline. Effects on guinea-pig atria (beta 1) are negligible and those on guinea-pig trachea (beta 1 and beta 2) and cat atria (beta 1 and beta 2) are equivalent to 40-50% of the maximum effects of isoprenaline. It is concluded that the intrinsic sympathomimetic activity of pindolol is exerted principally on the beta 2-adrenoceptor. The beta-adrenoceptor blocking effect of pindolol is largely confined to the (-)enantiomer, whereas its stimulant effects are shared equally by the (+) and (-)enantiomers. Removal of the side chain hydroxyl group of pindolol does not diminish stimulant activity, but abolishes blocking activity. Pindolol-induced stimulation and blockade of beta-adrenoceptors may be brought about by different configurations of the molecule. Vasodilator effects observed in vitro and in vivo suggest that beta-adrenoceptor stimulation may make an important contribution to the antihypertensive effect of pindolol in man.

Animals↗
PubMed2005

Pindolol is a potent scavenger of reactive nitrogen species.

Pindolol is an indolic drug that has been shown to enhance and/or accelerate selective serotonin specific reuptake inhibitors (SSRI)-induced antidepressant (AD) effect, even though the respective mechanism is still unclear. It has been demonstrated that inhibition of nitric oxide (*NO) synthesis in CNS produces anxiolytic and AD-like behavioural effects in a variety of animal paradigms. On the other hand, sustained high levels of *NO may be deleterious to CNS, predominantly due to the formation of peroxynitrite anion (ONOO-), which is generated via reaction of *NO with superoxide radical (O2*-). Therefore, the purpose of the present study was to characterize the putative pindolol scavenging effect on *NO, ONOO-, and O2*-, using in vitro non-cellular systems. The obtained results clearly show that pindolol is a potent scavenger of *NO (IC50 of 449+/-33 microM) and ONOO- (IC50 of 131+/-24 microM). Additionally, the scavenging effect of pindolol increased almost 8 times in the presence of 25 mM NaHCO3 (IC50 of 17+/-3 microM), which indicates that pindolol efficiently scavenges reactive species that are produced from the ONOO-/CO2 reaction such as the nitrogen dioxide radical (*NO2) and the carbonate radical anion (CO3*-). These effects may contribute for the reduction of SSRI antidepressant latency that has been attributed to pindolol and may also constitute an additional value for this drug when depression is associated with pro-oxidant neurodegenerative diseases.

Antidepressive Agents, Second-Generation↗
PubMed2004

Attenuation of the effects of fluoxetine on serotonergic neuronal activity by pindolol in rats.

Based on its proposed ability to block the effect of selective serotonin reuptake inhibitors (SSRIs) on the firing rate of serotonergic neurons, the 5-HT1A partial agonist/beta-adrenergic antagonist pindolol has been examined in clinical trials for its ability to enhance the efficacy of SSRIs. However, varying results have been obtained in these clinical trials. To explore this issue, we examined the effects of pindolol alone and in combination with fluoxetine on the electrophysiological activity of serotonergic neurons in the dorsal raphe nucleus of anesthetized rats. Administration of pindolol (1, 5, and 20 mg/kg, s.c.) alone decreased the number of spontaneously active serotonergic neurons. Administration of fluoxetine (10 mg/kg, i.p.) alone also decreased the number of spontaneously active serotonergic neurons. However, when administered following fluoxetine, pindolol significantly attenuated, but did not block completely, the inhibitory effects of fluoxetine on the number of spontaneously active serotonergic neurons. These results indicate that pindolol can attenuate the effects of fluoxetine on the firing of serotonergic neurons. These results may help explain the varying efficacy of pindolol in clinical trials with SSRIs.

Action Potentials↗
PubMed2004

Pindolol does not augment cortisol and prolactin responses to paroxetine in healthy subjects.

OBJECTIVE: Animal studies have shown that pindolol augmentation of selective serotonin re-uptake inhibitors (SSRIs) may act through inhibition of 5-HT(1A) autoreceptors in the raphe. The combination of pindolol plus a SSRI produces increased synaptic 5-HT levels that are greater than those achieved with a SSRI alone. However, it is unclear whether this actually occurs in humans, and clinical studies of pindolol augmentation have produced inconsistent results. Since the release of cortisol and prolactin is under serotonergic control, we hypothesized that pindolol augmentation of synaptic 5-HT concentrations produced by an SSRI in humans should lead to enhanced SSRI-induced cortisol and prolactin responses. METHODS: Cortisol and prolactin responses were measured after challenge tests with paroxetine (20-40 mg) plus pindolol (5 mg) and after paroxetine plus placebo in six non-depressed, healthy control subjects. RESULTS: No differences were observed in the cortisol or prolactin responses between either neuroendocrine challenge test. CONCLUSIONS: These results suggest that SSRI augmentation with usual clinical doses of pindolol does not increase central synaptic 5-HT neurotransmission sufficient to induce an enhanced neuroendocrine response.

Adrenergic beta-Antagonists↗
PubMed2000

Pindolol augmentation of antidepressant treatment: recent contributions from brain imaging studies.

Preclinical studies suggest that augmentation of selective serotonin (5-HT) reuptake inhibitors by the 5-HT(1A) receptor agent pindolol might reduce the delay between initiation of treatment and antidepressant response, an effect largely mediated by blockade of 5-HT(1A) autoreceptors in the dorsal raphe nuclei. Although some controlled clinical trials suggest that pindolol might reduce latency to selective serotonin reuptake inhibitor response in acute depressive episodes, the effect is moderate and highly variable. Recent positron emission tomography studies investigating the occupancy of 5-HT(1A) receptors in humans by pindolol have shown that at the dose used most often in clinical trials the occupancy is low and variable, which might explain the inconsistent clinical results. Positron emission tomography studies also suggest that pindolol might be more potent at blocking 5-HT(1A) autoreceptors than at blocking postsynaptic receptors, a property that may be useful in this pharmacologic strategy. Thus, the positron emission tomography data support the potential of pindolol to augment the antidepressant response of selective serotonin reuptake inhibitors, but also imply that this potential has not been fully evaluated. Here we review the clinical trials, the positron emission tomography studies, and the possible mechanisms of pindolol augmentation. It is also suggested that positron emission tomography may be used to define therapeutic dosing early on in the process of clinical evaluation of new treatment strategies.

Animals↗
PubMed2000

The role of 5-HT(1A) and 5-HT(1B/1D) receptors on the modulation of acute fluoxetine-induced changes in extracellular 5-HT: the mechanism of action of (+/-)pindolol.

Some clinical evidence has suggested that (+/-)pindolol can be effective at producing a shortened time to onset of antidepressant activity when co-administered with a serotonin specific reuptake inhibitor (SSRI). This effect has been attributed to the antagonist effects of pindolol at the 5-HT(1A) receptor. In the present study, we compared the pharmacology of (+/-)pindolol, WAY-100635 (a 5-HT(1A) antagonist), GR127935 (a 5-HT(1B/1D) antagonist), and isamoltane (a 5-HT(1B) antagonist), when given acutely in combination with fluoxetine, using in vivo microdialysis in the frontal cortex of the freely moving rat. We have determined that the acute fluoxetine-induced increases in extracellular 5-HT can be augmented by (+/-)pindolol, WAY100635, GR127935 and isamoltane with maximum increases of 216+/-32%, 235+/-49%, 240+/-18% and 171+/-47% of preinjection control levels, respectively. Combination of both 5-HT(1A) and 5-HT(1B/1D) autoreceptor antagonists with fluoxetine produced additive increases in extracellular 5-HT (i.e. WAY100635+GR127935+fluoxetine and WAY100635+isamoltane+fluoxetine produced a four- and five-fold potentiation, respectively), suggesting that this strategy may be useful in further augmenting the action of a SSRI in the treatment of depression. In addition, by comparing the combined administration of (+/-)pindolol with either WAY100635, GR127935 or isamoltane, we have determined that (+/-)pindolol produces much of its acute potentiation of fluoxetine-induced increases in extracellular 5-HT via its action at the 5-HT(1B/D) receptor in addition to any activity it has at the presynaptic 5-HT(1A) receptor.

Animals↗
PubMed1999

Sustained antidepressant effect of sleep deprivation combined with pindolol in bipolar depression. A placebo-controlled trial.

Total sleep deprivation (TSD) shows powerful but transient clinical effects in patients affected by bipolar depression. Pindolol blocks the serotonergic 5-HT1A autoreceptor, thus improving the antidepressant effect of selective serotonin reuptake inhibitors. We evaluated the interaction of TSD and pindolol in the treatment of acute episodes of bipolar depression. Forty bipolar depressed inpatients were randomized to receive pindolol 7.5 mg/day or placebo for nine days in combination with three consecutive TSD cycles. Pindolol significantly improved the antidepressant effect of TSD, and prevented the short-term relapse after treatment. The response rate (HDRS scores < 8) at the end of treatment was 15/20 for pindolol, and 3/20 for placebo. Coadministration of pindolol and TSD resulted in a complete response, which could be sustained for six months with lithium salts alone, in 65% of cases. This results suggest a major role for serotonergic transmission in the mechanism of action of TSD, and makes TSD treatment more effective in the treatment of bipolar depression.

Acute Disease↗
PubMed2000

Pindolol augmentation in treatment-resistant obsessive compulsive disorder: a double-blind placebo controlled trial.

OBJECTIVE: To evaluate the efficacy of pindolol augmentation in treatment-resistant obsessive compulsive disorder (OCD) patients who were unsuccessfully treated with serotonin reuptake inhibitors. METHOD: Fourteen treatment-resistant OCD patients were treated with paroxetine for 17.4+/-2.1 weeks up to 60 mg/d after they failed at least two other serotonin reuptake inhibitor trials. The patients, who did not respond to open-label paroxetine treatment, were assigned to a double-blind, placebo-controlled pindolol (2.5 mgx3/d) augmentation. All the subjects were evaluated biweekly for a six-week period with the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), Hamilton Anxiety Scale (HAM-Anx), and Montgomery Asberg Depression Rating Scale (MADRS). Data was analyzed by paired t-test, and ANOVA with repeated measures. RESULTS: Pindolol augmentation to paroxetine (n=8) as compared to placebo augmentation (n=6), was associated with a significant (P<0.01) improvement in Y-BOCS as measured by paired t-test after the fourth week of the treatment and by ANOVA with repeated measures (df: 4.9, f: 3,3, P<0.006). Although no significant differences were found between placebo and pindolol groups on HAM-Anx and MADRS, a trend for improvement in the pindolol group was noted. CONCLUSIONS: The results of our study demonstrated that pindolol may augment the therapeutic effect of paroxetine in treatment-resistant OCD patients.

Adolescent↗
PubMed1980

Effects of pindolol on renal function.

Because beta blockers have been shown to reduce glomerular filtration rate (GFR), the renal effect of intravenous and prolonged oral administration of pindolol was examined in 10 patients with essential hypertension. Intravenous pindolol decreased inulin clearance from 99 to 94 ml/min/1.73 m2 (p < 0.005), and pulse rate from 75 to 69/min (p < 0.005). Blood pressure and filtration fraction were not changed. Oral pindolol (10 to 20 mg/day) for a mean of 6 mo resulted in a decrease in mean blood pressure from 124 to 111 mm Hg (p < 0.001), in mean pulse rate from 76 to 69/min (p < 0.005), and in mean plasma renin activity (PRA) from 0.9 to 0.29 ng/ml/hr (p < 0.05). Inulin clearance and filtration fraction did not change. At the end of oral therapy, intravenous pindolol induced a greater reduction in inulin clearance than in the first study. These observations indicate that intravenous pindolol induces a decrease in GFR probably secondary to hemodynamic effects. On the other hand, prolonged oral pindolol has no effect on GFR despite decreases in blood pressure, pulse rate, and PRA.

Adult↗