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PubMed1990

Double-blind comparison of once daily betaxolol versus propranolol four times daily in stable angina pectoris. Betaxolol Investigators Group.

Betaxolol is a new, highly cardioselective, once-a-day beta blocker with a long half-life (mean 16 hours). The antianginal efficacy of 2 doses of betaxolol (20 and 40 mg) given once daily was evaluated and compared with propranolol (40 or 80 mg) 4 times daily. Ninety-two patients completed the 10-week double-blind trial. The resting and exercise heart rate, blood pressure and double product were similar for all treatment arms of the study during placebo treatment. Significant decreases in these measures occurred during active drug treatment when compared with placebo. No significant intergroup differences were noted at rest. Maximal exercise heart rate and double product were significantly lower during treatment with betaxolol 40 mg daily than in the propranolol 40 mg 4 times/day treatment group (p less than 0.05). All patients had chest pain and greater than or equal to 1 mm of ST-segment depression during the baseline placebo exercise test. After 10 weeks of active treatment, 55% of the patients were free of chest pain during maximal exercise (difference not significant between treatments). In the betaxolol 40 mg/day group, fewer (6 of 19; 32%) of the patients developed ST-segment depression with exercise (p less than 0.05) compared with propranolol 80 mg 4 times daily (21 of 26; 81%). Betaxolol appears to be a useful once-a-day cardioselective beta blocker for the therapy of angina pectoris.

Angina Pectoris↗
PubMed1990

A double-masked three-month comparison between 0.25% betaxolol suspension and 0.5% betaxolol ophthalmic solution.

In 352 patients with primary open-angle glaucoma or ocular hypertension, a multicenter double-masked, parallel-group clinical study compared the effects on intraocular pressure and ocular comfort of 0.5% betaxolol ophthalmic solution, a cardioselective beta-adrenergic blocking agent, with 0.25% betaxolol suspension. With twice-daily dosages, baseline intraocular pressure was significantly reduced (P = .0005), with no significant difference between the two groups, at Week 2 and at Months 1, 2, and 3. Further, the prevalence of ocular discomfort upon topical instillation was significantly lower for 0.25% betaxolol suspension than for 0.5% betaxolol solution (P = .0005).

Administration, Topical↗
PubMed1989

Changing therapy from timolol to betaxolol. Effect on intraocular pressure in selected patients with glaucoma. Timolol-Betaxolol Study Group.

Three hundred fifty-three patients whose intraocular pressure was controlled with a timolol maleate ophthalmic solution were studied. Following a baseline period, half were switched (masked and randomized) to treatment with a betaxolol hydrochloride ophthalmic solution and were followed up for 12 weeks. Intraocular pressure, signs, and symptoms were recorded at weeks 1, 4, 8, and 12. Those patients switched to the betaxolol ophthalmic solution had a significant increase in both ocular side effects (burning/stinging and tearing) and intraocular pressure at weeks 4, 8, and 12 when compared with those patients who continued to receive timolol.

Adrenergic beta-Antagonists↗
PubMed2001

Vasorelaxant effects of racemic betaxolol and its R- and S- isomers on bovine retinal vessels.

PURPOSE: RS-Betaxolol (equimolar R- and S- isomers) lowers intraocular pressure and dilates precontracted retinal and posterior ciliary arteries in vitro. Betaxolol's vasorelaxant effect is thought to involve the inhibition of calcium influx into vascular smooth muscle and is unrelated to its stereoselective beta-adrenergic blocking action. The authors assessed the vasodilatory effect of RS-betaxolol on different diameters of bovine retinal arterioles and venules, and these responses were compared with the responses induced by R- and S-betaxolol isomers in vitro. METHOD: In-vitro preparations of the bovine retinal microcirculatory system were perfused continuously with oxygenated, heparinized physiological salt solution at 37 degrees C. Diameters of retinal arterioles and venules were measured using video imaging. The retinal vessels were preconstricted with 40 mM KCl, and concentration-response curves for vasodilation were obtained for RS-betaxolol, R-betaxolol, and S-betaxolol. RESULTS: Baseline diameters of first-order (A1) and second-order (A2) branches of retinal arterioles were 50 +/- 0.6 microm and 39 +/- 1 microm, respectively (n = 20), whereas diameters of first-order (V1) and second-order (V2) branches of venules were 75 +/- 0.8 microm and 50 +/- 0.4 mM, respectively (n = 20). The diameters of all sizes of retinal arterioles and venules were significantly reduced (i.e., vasoconstricted) in the presence of 40 mM KCl (n = 20). These preconstricted vessels were relaxed in a dose-dependent manner by cumulative additions of RS-betaxolol, R-betaxolol, and S-betaxolol. The dose-response curves of these compounds were not significantly different. CONCLUSION: RS-Betaxolol, R-betaxolol, and S-betaxolol were equiactive and produced concentration-dependent vasodilatation of all sizes of retinal arterioles and venules studied.

Adrenergic beta-Antagonists↗
PubMed2000

Suppressive actions of betaxolol on ionic currents in retinal ganglion cells may explain its neuroprotective effects.

Betaxolol, a beta 1-selective adrenoceptor antagonist, is widely used in the treatment of glaucoma. In addition to its ocular hypotensive effects, betaxolol has been suggested to act as a retinal neuroprotective agent (Osborne et al., 1997). To investigate possible mechanisms underlying the neuroprotective effects, we tested the actions of betaxolol on ion channels and calcium signaling in isolated retinal ganglion cells. Betaxolol (50 microM) reduced by about 20% the high-voltage-activated (HVA) Ca channel currents in ganglion cells isolated from tiger salamander retina. In contrast, the beta 1-adrenoceptor antagonists propranolol (10 microM) and timolol (50 microM) had no inhibitory actions on HVA Ca channel currents. The L-type Ca channel antagonist, nisoldipine, blocked the HVA Ca channel current partially and the remaining current was not inhibited by betaxolol. Outward current was inhibited in the presence of betaxolol. Both iberiotoxin (IBTX; 10 nM), a selective inhibitor of large-conductance Ca-activated K channels, and Cd2+ (100 microM), which suppresses Ca-activated K channels subsequent to its block of Ca channels, reduced outward current and the remaining current was not blocked significantly with betaxolol. In the presence of betaxolol, Na channel currents were reduced by about 20%, as were currents evoked by glutamate (10 mM) and GABA (1 mM). Current clamp recordings from isolated ganglion cells showed that betaxolol had several effects on excitability: spike height decreased, repetitive spike activity was suppressed, spike width increased and hyperpolarization following spikes was reduced. Calcium imaging in isolated rat retinal ganglion cells revealed that betaxolol inhibited glutamate-induced increases in [Ca2+]i. These results suggest that betaxolol has a diversity of suppressive actions on ganglion cell ion channels and that, as a consequence, one of the net actions of the drug is to reduce Ca2+ influx. The subsequent reduction in [Ca2+]i may contribute to the apparent neuroprotective actions of betaxolol in promoting ganglion cell survival following ischemic insult, as may occur in glaucoma and retinal disease.

Action Potentials↗
PubMed1998

Aqueous humour concentration and the intraocular pressure-lowering effect of topical betaxolol before cataract surgery.

OBJECTIVE: The aim was to study the relationship between aqueous humour betaxolol concentration and intraocular pressure (IOP). METHODS: In this double-blind, randomized study, we administered betaxolol (a) or placebo (b) ocularly to 131 patients scheduled for cataract surgery. The patients were randomly divided into ten groups. In groups 1a and 1b, the drug was scheduled to be instilled 1-2 h, in groups 2a and 2b 12 h, in groups 3a and 3b 24 h, and in groups 4a and 4b 48 h before surgery. The pupil was dilated in all eyes prior to surgery. The IOP was measured with Perkins' applanation tonometer before the instillation of the drug and just before the peribulbar block. Twenty microlitres of 0.5% betaxolol or placebo solution was instilled into the eye. IOP was also measured before instillation of the drug and after 1 2 h in undilated eyes of 20 patients, whose contralateral eye was to be operated on, to rule out the effect of pupil dilation on IOP (groups 5a and 5b). Aqueous humour betaxolol concentrations were analysed using a radioreceptor assay. RESULTS: Betaxolol did not decrease IOP significantly in eyes with pupillary dilation. Both betaxolol and placebo decreased IOP significantly in patients without pupillary dilation, the effect of betaxolol being slightly more pronounced. The betaxolol concentration in aqueous humour was 731 ng m-1 in group la, 2.4 h after drug instillation. Measurable concentrations of betaxolol were also detected in aqueous humour in group 4a 47.7 h after drug administration. CONCLUSION: No correlation between aqueous humour concentration of betaxolol and the effect on IOP was found in eyes where the pupil was dilated before surgery. A single betaxolol dose did not decrease IOP significantly in patients undergoing cataract surgery, but the IOP decreasing effect was, however, clearly seen in patients who did not receive mydriatic drugs. The routine use of topical betaxolol prior to cataract surgery to decrease IOP is not recommended.

Adrenergic beta-Antagonists↗
PubMed2006

Concentrations of betaxolol in ocular tissues of patients with glaucoma and normal monkeys after 1 month of topical ocular administration.

PURPOSE: To measure the concentration of betaxolol in tissues of humans with glaucoma and normal monkeys after topical administration. METHODS: Enucleated eyes (n = 7) of patients with glaucoma (age range, 27-79 years), without apparent anatomic disruption that would be likely to influence betaxolol absorption and intraocular distribution (exceptions: one pseudophakic, one aphakic) or other disease, were analyzed for betaxolol concentrations after self-administration of 0.25% betaxolol twice daily for 28 days or longer. The last instillation was made within 6 hours of surgery. Cynomolgus monkeys (n = 3) received 0.25% betaxolol twice daily unilaterally for 30 days. Betaxolol was measured by HPLC and tandem mass spectrometry (MS/MS) in plasma and ocular tissues. RESULTS: In humans, mean betaxolol concentrations (excluding the aphakic patient) were 71.4 +/- 41.8 ng/g in the retina, 31.2 +/- 14.8 ng/g in the optic nerve head, and 1290 +/- 1170 ng/g in the choroid. Mean concentrations in the iris and ciliary body were 73,200 +/- 89,600 and 4,250 +/- 3,020 ng/g, respectively. Betaxolol concentration was higher in all ocular tissues than in the plasma (0.59 +/- 0.32 ng/mL). In the monkeys the concentrations in the posterior tissues of the treated eyes were higher than in the untreated eyes, with mean differences in the retina and optic nerve head of 121 and 130 ng/g, respectively. CONCLUSIONS: Topically applied betaxolol was bioavailable to posterior ocular tissues, including the retina and optic nerve head, of patients with glaucoma and of normal cynomolgus monkeys. The higher betaxolol levels in the treated versus untreated monkey eyes are consistent with betaxolol's reaching posterior tissues by local absorption and distribution.

Administration, Topical↗
PubMed1990

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

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

Animals↗
PubMed2003

Betaxolol-induced deterioration of asthma and a pharmacodynamic analysis based on beta-receptor occupancy.

OBJECTIVE: To report a case of deterioration of asthma associated with continuous use of oral betaxolol, a beta1-selective beta-blocking agent. We also analyzed the pharmacokinetics in this case by applying a receptor occupancy model. CASE SUMMARY: A 68-year-old woman taking 5 mg of betaxolol for hypertension occasionally experienced asthmatic coughing after upper respiratory tract infection. Two years after the start of betaxolol, her asthma gradually worsened. Although pharmacotherapy for asthma was introduced, betaxolol was continued. Finally, she was admitted to hospital with bronchospasm. When she was discharged after 2 months, betaxolol was discontinued and losartan potassium (25 mg/d) was initiated instead for her hypertension. Since then, she has been free from bronchospasm. METHOD: We calculated the mean receptor occupancy (phiSS) of the beta1- and beta2-receptors after the usual oral dose of betaxolol by using pharmacokinetic-pharmacodynamic parameters obtained from the literature. We estimated the decrease in the exercise pulse rate or the forced expiratory volume in 1 second (FEV1) by applying the phiSS values to the model previously reported by us. RESULTS: Betaxolol seems less likely than other beta1-blocking agents to cause pulmonary adverse effects. However, the estimated decrease in FEV1 after oral administration of betaxolol (5 mg) was close to that after oral bisoprolol (5 mg), which has been reported to induce asthma. CONCLUSIONS: Oral betaxolol may induce bronchospasm, although betaxolol is considered to be highly cardioselective and seems less likely than other beta1-selective blocking agents to cause pulmonary adverse effects. Betaxolol should be administered with caution to patients with asthma or chronic pulmonary disease.

Administration, Oral↗
PubMed2000

Effects of betaxolol on light responses and membrane conductance in retinal ganglion cells.

PURPOSE: To examine the physiological effects of betaxolol, a beta1-adrenergic receptor blocker commonly used in the treatment of glaucoma, on retinal ganglion cells and to evaluate its potential to elicit responses consistent with a neuroprotective agent against ganglion cell degeneration. METHODS: Single-unit extracellular recording, electroretinogram (ERG), intracellular and whole-cell patch-clamp recording techniques were made from flatmounted, isolated retina, superfused eyecup, and living retinal slice preparations of the larval tiger salamander. RESULTS: Bath application of 20 microM betaxolol reduced the glutamate-induced increase of spontaneous spike rate in retinal ganglion cell by approximately 30%. The glutamate-induced postsynaptic current recorded under voltage-clamp conditions was reduced by 50 microM betaxolol, and the difference current-voltage (I-V) relation (I(Control)-I(betaxolol)) was N-shaped and AP5-sensitive, characteristic of N-methyl-D-aspartate receptor-mediated current. Application of 50 microM betaxolol reversibly reduced the voltage-gated sodium and calcium currents by approximately one third of their peak amplitudes. The times-to-action of betaxolol on ganglion cells are long (15-35 minutes for 20-50 microM betaxolol), indicative of modulation through slow biochemical cascades. Betaxolol, up to 100 microM, exerted no effects on horizontal cells or the ERG, suggesting that the primary actions of this beta1 blocker are restricted to retinal ganglion cells. CONCLUSIONS: These physiological experiments provide supporting evidence that betaxolol acts in a manner consistent with preventing retinal ganglion cell death induced by elevated extracellular glutamate or by increased spontaneous spike rates under pathologic conditions. The physiological actions of betaxolol lead to reducing neurotoxic effects in ganglion cells, which are the most susceptible retinal neurons to glutamate-induced damages under ischemic and glaucomatous conditions. Therefore, betaxolol has the potential to be a neuroprotective agent against retinal degeneration in patients with disorders mediated by such mechanisms.

Adrenergic beta-Antagonists↗
PubMed2005

Beta1-adrenergic receptor polymorphisms and clinical efficacy of betaxolol hydrochloride in normal volunteers.

OBJECTIVE: To evaluate the relationship between polymorphisms in the gene encoding the beta1-adrenergic receptor (beta1-AR) and clinical response to betaxolol hydrochloride 0.25% in a small pilot study of normal volunteers. DESIGN: Prospective nonrandomized comparative trial. PARTICIPANTS: Forty-eight consecutive normal volunteers who met all eligibility requirements for inclusion into this study. METHODS: Baseline intraocular pressure (IOP) was recorded. Subjects began treatment with betaxolol (1 drop both eyes twice daily) and underwent follow-up IOP recordings at 3 and 6 weeks. Peripheral blood was obtained for genetic analysis. MAIN OUTCOME MEASURES: Response to betaxolol was calculated as the change in mean IOP from baseline (averaged between both eyes and averaged between both follow-up visits). The beta1-AR genotype was determined by polymerase chain reaction with restriction fragment length polymorphisms at codons 49 (serine [Ser] or glycine [Gly]) and 389 (arginine [Arg] or Gly). RESULTS: There were 32 Ser49 homozygotes and 16 Gly49 carriers. There were no statistically significant differences between the Ser49 homozygotes and the Gly49 carriers with respect to baseline IOP or response to betaxolol therapy. There were 25 Arg389 homozygotes and 23 Gly389 carriers (22 heterozygotes and 1 Gly389 homozygote). As compared with Gly389 carriers, the Arg389 homozygotes had a higher baseline IOP (15.8 mmHg vs. 13.7 mmHg; P = 0.009) and a greater magnitude of response to betaxolol therapy (-3.4 mmHg vs. -1.5 mmHg; P = 0.0009). The Ser49 homozygote genotype was not independently associated with baseline IOP (P = 0.47) or with a response to betaxolol (P = 0.99). The Arg389 homozygote genotype was independently associated with a higher baseline IOP (P = 0.03) and a greater response to betaxolol (P = 0.03), even after adjusting for baseline IOP. CONCLUSIONS: In this small pilot series, a single nucleotide polymorphism at codon 389 in the beta1-AR seems to correlate with a response to betaxolol therapy in normal, nonglaucomatous volunteers. There was no such correlation at codon 49. The polymorphism at codon 389 may predict short-term response to betaxolol and may serve as a determinant of response to betaxolol and other adrenergic agents in glaucomatous eyes requiring treatment.

Adrenergic beta-Antagonists↗
PubMed2001

Comparison of the clinical success and quality-of-life impact of brimonidine 0.2% and betaxolol 0.25 % suspension in patients with elevated intraocular pressure.

BACKGROUND: Brimonidine tartrate 0.2%, a selective alpha2-adrenergic receptor agonist, and betaxolol 0.25% suspension, a cardioselective beta1-adrenergic receptor antagonist, are used in the treatment of elevated intraocular pressure (IOP). OBJECTIVE: This study compared the clinical success and quality-of-life impact of 4 weeks of treatment with brimonidine 0.2% BID compared with those of 4 weeks of treatment with betaxolol 0.25% suspension BID in patients with elevated IOP. METHODS: This was a multisite, double-masked, comparative clinical trial in patients with glaucoma or ocular hypertension. Patients were randomly assigned to receive either brimonidine or betaxolol BID. Morning IOP was measured at baseline and at weeks 1 and 4 using Goldmann applanation. Efficacy was determined by reduction in IOP from baseline. Patients experiencing a > or =20% reduction in IOP were considered to have a successful IOP-lowering response. The Glaucoma Disability Index questionnaire was administered at week 4 to assess quality-of-life factors and the incidence of adverse events. Ophthalmic examinations were conducted at each visit. RESULTS: One hundred fifty-nine patients were randomized to treatment and completed the study, 81 receiving brimonidine and 78 receiving betaxolol. The majority were white (77.4%) and female (61.6%), and had a diagnosis of open-angle glaucoma (56.0%). After 4 weeks of treatment, both brimonidine and betaxolol effectively lowered IOP from baseline (mean IOP reductions: brimonidine, 5.96 mm Hg; betaxolol, 5.07 mm Hg; P = NS). However, a significantly higher percentage of brimonidine patients (52/81 [64.2%]) than betaxolol patients (37/78 [47.4%]) had a > or =20% reduction in IOP (P = 0.033). No serious adverse events were reported with either study medication. On the quality-of-life assessments, more betaxolol patients reported hyperemia (P = 0.011), and the reported hyperemia was significantly more severe in betaxolol patients (P = 0.009). CONCLUSIONS: After 4 weeks of treatment, brimonidine 0.2% BID was clinically successful in significantly more patients and was better tolerated than 4 weeks of treatment with betaxolol 0.25% BID in this population.

Adrenergic alpha-Agonists↗
PubMed2000

Betaxolol, a beta(1)-adrenoceptor antagonist, reduces Na(+) influx into cortical synaptosomes by direct interaction with Na(+) channels: comparison with other beta-adrenoceptor antagonists.

Betaxolol, a beta(1)-adrenoceptor antagonist used for the treatment of glaucoma, is known to be neuroprotective in paradigms of ischaemia/excitotoxicity. In this study, we examined whether betaxolol and other beta-adrenoceptor antagonists interact directly with neurotoxin binding to sites 1 and 2 of the voltage-sensitive sodium channel (Na(+) channel) in rat cerebrocortical synaptosomes. Betaxolol inhibited specific [(3)H]-batrachotoxinin-A 20-alpha-benzoate ([(3)H]-BTX-B) binding to neurotoxin site 2 in a concentration-dependent manner with an IC(50) value of 9.8 microM. Comparison of all the beta-adrenoceptor antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>levobunolol approximately carteolol>/=timolol>atenolol. None of the drugs caused a significant inhibition of [(3)H]-saxitoxin binding to neurotoxin receptor site 1, even at concentrations as high as 250 microM. Saturation experiments showed that betaxolol increased the K(D) of [(3)H]-BTX-B binding but had no effect on the B(max). The association kinetics of [(3)H]-BTX-B were unaffected by betaxolol, but the drug significantly accelerated the dissociation rate of the radioligand. These findings argue for a competitive, indirect, allosteric mode of inhibition of [(3)H]-BTX-B binding by betaxolol. Betaxolol inhibited veratridine-stimulated Na(+) influx in rat cortical synaptosomes with an IC(50) value of 28. 3 microM. Carteolol, levobunolol, timolol and atenolol were significantly less effective than betaxolol at reducing veratridine-evoked Na(+) influx. The ability of betaxolol to interact with neurotoxin site 2 of the Na(+) channel and inhibit Na(+) influx may have a role in its neuroprotective action in paradigms of excitotoxicity/ischaemia and in its therapeutic effect in glaucoma.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2002

[Human trabecular cells and apoptosis: in vitro evaluation of the effect of betaxolol with or without preservative].

PURPOSE: Trabecular meshwork, which is involved in aqueous outflow resistance, is deeply modified in glaucoma patients, with a decrease in the trabecular cell number. Trabecular toxicity of antiglaucoma medications cannot be excluded. On a human cultured trabecular cell line, we investigated the potential proapoptotic effect of a beta-blocker with or without preservative, benzalkonium chloride (0.01% BAC), by flow cytometry and confocal microscopy. MATERIAL: and METHODS: A human immortalized trabecular cell line (HTM-5) obtained from a normal donor was cultured under normal conditions. Preserved 0.25% betaxolol suspension (betaxolol BAC +), unpreserved 0.25% betaxolol suspension, and 0.01% BAC were respectively added to the culture medium in a 1/10 or 1/100 dilution for 15 minutes. After a 24-hour recovery period in normal culture conditions, cell size and the expression of an apoptotic marker, Apo 2.7, were evaluated by flow cytometry and confocal microscopy. Untreated trabecular cells were used as control cells. RESULTS: Preserved and unpreserved betaxolol in a 1/10 dilution induced a significant decrease in trabecular cell size compared to controls. However, this cell size decrease was less pronounced than that induced by BAC at the same dilution. Similar results were obtained with betaxolol and BAC in a 1/100 dilution. Trabecular cell Apo 2.7 expression was significantly increased after treatment with betaxolol BAC + and BAC- in a 1/10 dilution compared to controls (36.8%, 28.1%, and 15.4%, respectively p<0.005). However, this proapoptotic activity was much less pronounced than that induced by BAC- at the same dilution (96.9%, p<10(-4)). Unpreserved betaxolol in a 1/100 dilution had no apoptotic activity on trabecular cells. Trabecular cell Apo 2.7 expression slightly increased with betaxolol BAC + at a 1/100 dilution (24.9%, p=0.04), while it was greatly increased with BAC at the same dilution (39.9%; p<10(-4)). CONCLUSION: In our model, unpreserved betaxolol at a low concentration displayed no proapoptotic activity on trabecular cells. On the other hand, preserved betaxolol displayed a moderate proapoptotic activity by triggering cell death of around 25% of cells. Trabecular cell toxicity appeared to be mainly due to the preservative benzalkonium chloride (BAC). Taken together, our results demonstrated that the strong apoptotic activity of BAC was greatly reduced within the preserved eye drops, probably through the interaction of BAC with the active compound.

Adrenergic beta-Antagonists↗
PubMed1992

Dose-dependent effects of betaxolol in hypertension: a double-blind, multicenter study.

This study determined the dose-response relationship among three doses of betaxolol compared with placebo in patients with mild-to-moderate hypertension. In this double-blind, placebo-controlled trial, 317 hypertensive patients were randomly assigned to receive placebo or betaxolol 5, 10, or 20 mg once daily for 4 weeks. A significant (P less than .05) decrease in supine diastolic blood pressure (BP) compared with concurrent placebo was evident with all three doses of betaxolol after 1 week of active treatment. Each dose of betaxolol maintained a significant reduction in diastolic and systolic BP and heart rate responses throughout the 4-week treatment period. At the fourth week (final treatment evaluation), BP and heart rate were significantly (P less than .05) reduced by all three doses of betaxolol compared with placebo. For supine systolic and diastolic BP, the decreases with betaxolol 20 mg were significantly (P less than .05) greater than with the 5 mg dose, but there was no statistically significant difference between the 10-mg and either the 5- or 20-mg doses. For standing diastolic BP, the effect of betaxolol 5 mg once daily was significantly (P less than .05) less than that of 10 and 20 mg. The overall supine diastolic BP response to betaxolol was dose dependent, and more patients responded to the 10- and 20-mg doses of betaxolol (66% and 76%, respectively) than to the 5-mg dose (59%). For each efficacy variable, the absolute magnitude of the reduction was greater with increasing dose. In subgroup analyses, BP responses were analyzed by race, age, baseline BP, and age combined with baseline BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Topically applied betaxolol attenuates ischaemia-induced effects to the rat retina and stimulates BDNF mRNA.

It has previously been reported that the beta(1)-adrenoceptor antagonist, betaxolol, can protect retinal neurones from ischaemia when applied topically. It has further been shown that betaxolol can reduce influx of both sodium or calcium into neurones through interaction at neurotoxin site 2 of the sodium channel and the L-type calcium channel, respectively. The present study sought to further investigate the neuroprotective mode of action of betaxolol in the rat retina. Rats were treated topically with L-betaxolol for 10, 5 and 1 min before ischaemia, induced by raising the intraocular pressure above systolic blood pressure for 45 min. This was followed by reperfusion of 3 or 5 days where L-betaxolol was applied topically twice daily. Ischaemia plus reperfusion caused both a loss of immunoreactivity for choline acetyl transferase (ChAT) and a marked reduction of the b-wave of the electroretinogram (ERG). Treatment, as described, with topical L-betaxolol, completely blunted the effects upon ChAT immunoreactivity and caused a significant reversal of the ERG changes. Furthermore, other rats treated topically with commercially available racemic betaxolol (Betoptic Solution, 0.5%) for 6 hr had raised levels of mRNA for brain derived neurotrophic factor (BDNF) but not for basic fibroblast growth factor (bFGF) in their retinas. The combined data provide further evidence that betaxolol can blunt the effects of ischaemia to the rat retina when applied topically just before the insult. Furthermore, the finding that retinal levels of BDNF mRNA are raised following topical betaxolol treatment shows that not only can this drug reach the retina but that it can also induce changes in expression of factors which are known, themselves, to provide neuroprotection to retinal neurones.

Adrenergic beta-Antagonists↗
PubMed1986

Electrical stimulation releases 3H-betaxolol from rat atrial slices: possible role of noradrenergic nerves.

Under in vitro conditions, 3H-betaxolol was accumulated in rat atrial slices, reaching a tissue-medium ratio of 12.3 +/- 1.8 ml/g. This process was temperature-dependent, but ouabain-resistant. 3H-Betaxolol accumulated in atrial slices was subsequently released by electrical stimulation. The electrically-evoked release of 3H-betaxolol was abolished in the absence of calcium, and reduced in the presence of bretylium 10 microM. After surgical sympathetic denervation by stellate ganglionectomy there was a marked reduction in the endogenous content of noradrenaline and in the retention of 3H-noradrenaline in atrial slices. The concomitant decrease in the amount of 3H-noradrenaline released by electrical stimulation following denervation was modest, although statistically significant. Following sympathetic denervation, the tissue retention of 3H-betaxolol was not significantly affected, but the release of 3H-betaxolol by electrical stimulation was considerably reduced. After pretreatment with reserpine the amount of radioactivity released by electrical stimulation from slices labelled with 3H-betaxolol or 3H-noradrenaline was markedly reduced. The tissue retention of 3H-noradrenaline was reduced to a larger extent than that of 3H-betaxolol following the administration of reserpine. The simultaneous release of noradrenaline and betaxolol by nerve stimulation observed under our experimental conditions may represent a mechanism through which betaxolol can reach selectively the postsynaptic beta 1-adrenoceptors and reinforce beta-adrenoceptor blockade in the heart.

Adrenergic beta-Antagonists↗
PubMed1988

Long-term betaxolol therapy in glaucoma patients with pulmonary disease.

We evaluated the use of topically administered betaxolol 0.5% in 101 glaucoma patients (47 men and 54 women) who had chronic obstructive pulmonary disease, asthma, or timolol-induced bronchoconstriction. Betaxolol 0.5% was administered twice daily and patients were reexamined at three-month intervals for up to two years. In addition to measurement of intraocular pressure, pulmonary function tests were obtained before therapy (baseline), two or three weeks after initiating betaxolol therapy, and at yearly intervals. Before treatment with betaxolol, the mean ratio of forced expiratory volumes in one second (FEV1) to forced vital capacity (FVC) was 66.3% (n = 101). After two weeks of betaxolol treatment, mean FEV1/FVC ratio was 66.2% (n = 101). After one year of betaxolol therapy, mean FEV1/FVC ratio was 60.1% (n = 24), and after two years it was 54.4% (n = 5). Nine patients developed symptoms that may have been associated with betaxolol treatment and were withdrawn from the study. Five of these patients developed symptomatic pulmonary obstruction between one and 554 days after initiating betaxolol treatment. Topically administered betaxolol was well tolerated by most glaucoma patients with concomitant pulmonary disease.

Aged↗