Timolol: A beta-adrenergic antagonist similar in action to PROPRANOLOL. The levo-isomer is the more active. Timolol has been proposed as an antihypertensive, antiarrhythmic, antiangina, and antiglaucoma agent. It is also used in the treatment of MIGRAINE DISORDERS and tremor.Ophthalmic Solutions: Sterile solutions that are intended for instillation into the eye. It does not include solutions for cleaning eyeglasses or CONTACT LENS SOLUTIONS.Prostaglandins F, Synthetic: Analogs or derivatives of prostaglandins F that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGF.Intraocular Pressure: The pressure of the fluids in the eye.Ocular Hypertension: A condition in which the intraocular pressure is elevated above normal and which may lead to glaucoma.Betaxolol: A cardioselective beta-1-adrenergic antagonist with no partial agonist activity.Administration, Topical: The application of drug preparations to the surfaces of the body, especially the skin (ADMINISTRATION, CUTANEOUS) or mucous membranes. This method of treatment is used to avoid systemic side effects when high doses are required at a localized area or as an alternative systemic administration route, to avoid hepatic processing for example.Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.Glaucoma, Open-Angle: Glaucoma in which the angle of the anterior chamber is open and the trabecular meshwork does not encroach on the base of the iris.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Benzalkonium Compounds: A mixture of alkylbenzyldimethylammonium compounds. It is a bactericidal quaternary ammonium detergent used topically in medicaments, deodorants, mouthwashes, as a surgical antiseptic, and as a as preservative and emulsifier in drugs and cosmetics.Preservatives, Pharmaceutical: Substances added to pharmaceutical preparations to protect them from chemical change or microbial action. They include ANTI-BACTERIAL AGENTS and antioxidants.Cloprostenol: A synthetic prostaglandin F2alpha analog. The compound has luteolytic effects and is used for the synchronization of estrus in cattle.Aqueous Humor: The clear, watery fluid which fills the anterior and posterior chambers of the eye. It has a refractive index lower than the crystalline lens, which it surrounds, and is involved in the metabolism of the cornea and the crystalline lens. (Cline et al., Dictionary of Visual Science, 4th ed, p319)Metipranolol: A beta-adrenergic antagonist effective for both beta-1 and beta-2 receptors. It is used as an antiarrhythmic, antihypertensive, and antiglaucoma agent.Carteolol: A beta-adrenergic antagonist used as an anti-arrhythmia agent, an anti-angina agent, an antihypertensive agent, and an antiglaucoma agent.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Glaucoma: An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)ThiophenesProstaglandins, Synthetic: Compounds obtained by chemical synthesis that are analogs or derivatives of naturally occurring prostaglandins and that have similar activity.Fluorophotometry: Measurement of light given off by fluorescein in order to assess the integrity of various ocular barriers. The method is used to investigate the blood-aqueous barrier, blood-retinal barrier, aqueous flow measurements, corneal endothelial permeability, and tear flow dynamics.Conjunctiva: The mucous membrane that covers the posterior surface of the eyelids and the anterior pericorneal surface of the eyeball.Carbonic Anhydrase I: A cytosolic carbonic anhydrase isoenzyme primarily expressed in ERYTHROCYTES, vascular endothelial cells, and the gastrointestinal mucosa. EC 4.2.1.-Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.Pharmaceutical Vehicles: A carrier or inert medium used as a solvent (or diluent) in which the medicinally active agent is formulated and or administered. (Dictionary of Pharmacy, 1986)Sick Sinus Syndrome: A condition caused by dysfunctions related to the SINOATRIAL NODE including impulse generation (CARDIAC SINUS ARREST) and impulse conduction (SINOATRIAL EXIT BLOCK). It is characterized by persistent BRADYCARDIA, chronic ATRIAL FIBRILLATION, and failure to resume sinus rhythm following CARDIOVERSION. This syndrome can be congenital or acquired, particularly after surgical correction for heart defects.Vivisection: The cutting of or surgical operation on a living animal, usually for physiological or pathological investigation. (from Merriam-Webster's Collegiate Dict, 10th ed)Pacemaker, Artificial: A device designed to stimulate, by electric impulses, contraction of the heart muscles. It may be temporary (external) or permanent (internal or internal-external).Students, Pharmacy: Individuals enrolled in a school of pharmacy or a formal educational program leading to a degree in pharmacy.Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Blood Pressure Determination: Techniques for measuring blood pressure.Pressure: A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Protective Devices: Devices designed to provide personal protection against injury to individuals exposed to hazards in industry, sports, aviation, or daily activities.Phytotherapy: Use of plants or herbs to treat diseases or to alleviate pain.Urine Specimen Collection: Methods or procedures used to obtain samples of URINE.Drugs, Chinese Herbal: Chinese herbal or plant extracts which are used as drugs to treat diseases or promote general well-being. The concept does not include synthesized compounds manufactured in China.Night Vision: Function of the human eye that is used in dim illumination (scotopic intensities) or at nighttime. Scotopic vision is performed by RETINAL ROD PHOTORECEPTORS with high sensitivity to light and peak absorption wavelength at 507 nm near the blue end of the spectrum.Heart Failure: A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.Migraine Disorders: A class of disabling primary headache disorders, characterized by recurrent unilateral pulsatile headaches. The two major subtypes are common migraine (without aura) and classic migraine (with aura or neurological symptoms). (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)Headache: The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.Migraine with Aura: A subtype of migraine disorder, characterized by recurrent attacks of reversible neurological symptoms (aura) that precede or accompany the headache. Aura may include a combination of sensory disturbances, such as blurred VISION; HALLUCINATIONS; VERTIGO; NUMBNESS; and difficulty in concentrating and speaking. Aura is usually followed by features of the COMMON MIGRAINE, such as PHOTOPHOBIA; PHONOPHOBIA; and NAUSEA. (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)Sumatriptan: A serotonin agonist that acts selectively at 5HT1 receptors. It is used in the treatment of MIGRAINE DISORDERS.MaleatesDisposable Equipment: Apparatus, devices, or supplies intended for one-time or temporary use.Drug Information Services: Services providing pharmaceutic and therapeutic drug information and consultation.Drug Overdose: Accidental or deliberate use of a medication or street drug in excess of normal dosage.Drug Users: People who take drugs for a non-therapeutic or non-medical effect. The drugs may be legal or illegal, but their use often results in adverse medical, legal, or social consequences for the users.Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.Substance-Related Disorders: Disorders related to substance abuse.

Central injections of capsaicin cause antidiuresis mediated through neurokinin-1 receptors in rat hypothalamus and vasopressin release. (1/309)

Intracerebroventricular injections of capsaicin at 100-500 nmol elicited dose-dependent decreases in urine outflow volume in anesthetized, hydrated rats. The capsaicin (500 nmol)-induced antidiuresis was inhibited by pretreatment with CP96345 (30 nmol, a neurokinin-1-receptor antagonist), but not by that with phenoxybenzamine (20 nmol, an alpha-adrenoceptor antagonist), timolol (100 nmol, a beta-adrenoceptor antagonist) or atropine (300 nmol, a muscarinic antagonist) into the hypothalamic supraoptic nucleus (SON). Intravenous injections of d(CH2)5-D-Tyr(Et)VAVP (50 microg/kg, a vasopressin-receptor antagonist) completely blocked the antidiuresis. In intra-SON microdialysis experiments, acetylcholine concentration in the perfusate of the capsaicin-injected rats was not different from that of the vehicle-injected rats. These findings suggested that capsaicin stimulated substance P release in the SON and caused the antidiuresis as a result of the increased release of vasopressin into the circulation from the neurohypophysis mediated through neurokinin-1 receptors in the SON.  (+info)

Mitigation of caffeine-induced fetopathy in mice by pretreatment with beta-adrenergic blocking agents. (2/309)

In a previous experiment, fetopathic effects of caffeine were significantly reduced by pretreatment with propranolol at dosage levels of 2.5 to 10 mg/kg. The present experiments were undertaeken to investigate the relation between time intervals of propranolol pretreatment and its effect on reducing fetopathy. Furthermore, the effect of timolol, another beta-adrenergic blocking agent, on reducing fetopathy was compared with that of propranolol. Propranolol (5 mg/kg) administered 15, 30 or 60 minutes before caffeine treatment significantly reduced the caffeine-induced fetopathy. The optimal effect was found when propranolol was given 30 minutes before caffine. The reduction in fetopathy by timolol pretreatment was comparable to that of propranolol. The results lend support to the hypothesis that the fetopathic effect of caffeine is linked with released catecholamines in material or fetal issues of mice.  (+info)

Constitutively active mutants of the beta1-adrenergic receptor. (3/309)

We provide the first evidence that point mutations can constitutively activate the beta(1)-adrenergic receptor (AR). Leucine 322 of the beta(1)-AR in the C-terminal portion of its third intracellular loop was replaced with seven amino acids (I, T, E, F, C, A and K) differing in their physico-chemical properties. The beta(1)-AR mutants expressed in HEK-293 cells displayed various levels of constitutive activity which could be partially inhibited by some beta-blockers. The results of this study might have interesting implications for future studies aiming at elucidating the activation process of the beta(1)-AR as well as the mechanism of action of beta-blockers.  (+info)

Comparison of the intraocular pressure lowering effect of latanoprost and a fixed combination of timolol-pilocarpine eye drops in patients insufficiently controlled with beta adrenergic antagonists. French Latanoprost Study Group, and the Swedish Latanoprost Study Group. (4/309)

AIMS: To compare the effect on intraocular pressure (IOP) of latanoprost monotherapy and timolol-pilocarpine in patients with glaucoma or ocular hypertension with inadequately controlled IOP on topical beta adrenergic antagonists. METHODS: This was a multicentre, randomised, observer masked, 6 week study performed in France and Sweden. 23 centres enrolled 237 patients with glaucoma or ocular hypertension and an IOP of at least 22 mm Hg on treatment with topical beta adrenergic antagonists, alone or in combination. After a 21 day run in period on timolol 0.5% twice daily, patients were randomised either to latanoprost 0.005% once daily or to a fixed combination of timolol-pilocarpine twice daily. Changes in mean diurnal IOP from the baseline to the 6 week visit were determined with an analysis of covariance. RESULTS: Mean diurnal IOP was statistically significantly decreased from baseline in both groups (p<0.001). Switching to latanoprost treatment reduced mean diurnal IOP by 5.4 (SEM 0.3) mm Hg (ANCOVA -22%) and switching to timolol-pilocarpine treatment reduced mean diurnal IOP by 4.9 (0.4) mm Hg (-20%). Blurred vision, decreased visual acuity, decreased twilight vision, and headache were statistically significantly more frequent in the timolol-pilocarpine group. CONCLUSIONS: Latanoprost monotherapy was at least as effective as fixed combination timolol-pilocarpine twice daily treatment in reducing mean diurnal IOP in patients not adequately controlled on topical beta adrenergic antagonists. Latanoprost was better tolerated than timolol-pilocarpine regarding side effects. These results indicate that a switch to latanoprost monotherapy can be attempted before combination therapy is initiated.  (+info)

Effects of topical nipradilol, a beta blocking agent with alpha blocking and nitroglycerin-like activities, on intraocular pressure and aqueous dynamics in humans. (5/309)

AIMS: To study the effects of topical nipradilol, a non-selective beta blocker with alpha blocking and nitroglycerin-like activities, on intraocular pressure (IOP) and aqueous humour dynamics in normal humans and in patients with ocular hypertension. METHODS: Nipradilol (0.06%, 0.125%, 0.25%, 0.5%) was applied to normal volunteers (n = 12) to test for IOP lowering effects. In a second group of normal volunteers (n = 11), nipradilol (0.125% and 0.25%) and timolol (0. 5%) were compared for IOP lowering effects. After a single administration of 0.25% nipradilol, IOP, flare intensity in the anterior chamber, aqueous flow, uveoscleral outflow, tonographic outflow facility, and episcleral venous pressure were either directly measured or mathematically calculated. Topical nipradilol (0.25%) was administered to 24 patients with ocular hypertension twice daily for 8 weeks. RESULTS: Administration of 0.25% nipradilol decreased IOP with a maximum reduction of 4.2 mm Hg lasting 12 hours. A single instillation of both 0.25% nipradilol and 0.5% timolol reduced the IOP in normotensive human subjects to the same degree. A single instillation of 0.25% nipradilol decreased the aqueous flow rate in the treated eye by 20%. Nipradilol produced no significant effect in tonographic outflow facility or episcleral venous pressure, but uveoscleral outflow was increased. In patients with ocular hypertension, twice daily instillation of 0.25% nipradilol decreased IOP without tachyphylaxis for the 8 week test period. CONCLUSION: Topical nipradilol (0.25%) reduced IOP by decreasing the aqueous flow rate and probably also by increasing uveoscleral outflow. Nipradilol should be further investigated as a new antiglaucoma drug.  (+info)

Meal-induced insulin secretion in dogs is mediated by both branches of the autonomic nervous system. (6/309)

We investigated the relationship between autonomic activity to the pancreas and insulin secretion in chronically catheterized dogs when food was shown, during eating, and during the early absorptive period. Pancreatic polypeptide (PP) output, pancreatic norepinephrine spillover (PNESO), and arterial epinephrine (Epi) were measured as indexes for parasympathetic and sympathetic nervous activity to the pancreas and for adrenal medullary activity, respectively. The relation between autonomic activity and insulin secretion was confirmed by autonomic blockade. Showing food to dogs initiated a transient increase in insulin secretion without changing PP output or PNESO. Epi did increase, suggesting beta(2)-adrenergic mediation, which was confirmed by beta-adrenoceptor blockade. Eating initiated a second transient insulin response, which was only totally abolished by combined muscarinic and beta-adrenoceptor blockade. During absorption, insulin increased to a plateau. PP output showed the same pattern, suggesting parasympathetic mediation. PNESO decreased by 50%, suggesting withdrawal of inhibitory sympathetic neural tone. We conclude that 1) the insulin response to showing food is mediated by the beta(2)-adrenergic effect of Epi, 2) the insulin response to eating is mediated both by parasympathetic muscarinic stimulation and by the beta(2)-adrenergic effect of Epi, and 3) the insulin response during early absorption is mediated by parasympathetic activation, with possible contribution of withdrawal of sympathetic neural tone.  (+info)

Betaxolol, a beta(1)-adrenoceptor antagonist, reduces Na(+) influx into cortical synaptosomes by direct interaction with Na(+) channels: comparison with other beta-adrenoceptor antagonists. (7/309)

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.  (+info)

Effects of glaucoma medications on the cardiorespiratory and intraocular pressure status of newly diagnosed glaucoma patients. (8/309)

AIMS: To evaluate the short term cardiovascular, respiratory, and intraocular pressure (IOP) effects of four glaucoma medications in newly diagnosed glaucoma patients. METHODS: 141 newly diagnosed glaucoma patients were recruited and underwent a full ocular, cardiovascular, and respiratory examination, including an electrocardiogram (ECG) and spirometry. They were prescribed one of four topical glaucoma medications and reviewed 3 months later. One eye of each patient was randomly chosen for analysis, performed using analysis of variance and the chi(2) test. RESULTS: Latanoprost had the greatest mean IOP lowering effect in both the primary open angle glaucoma (POAG) (p = 0.005) and the "presumed" normal tension glaucoma (NTG) groups (p = 0.33), reducing the IOP by 8.9 mm Hg and 4.1 mm Hg respectively. Timolol was associated with lowered pulse rates and reductions in the spirometry measurements. 41% of patients using brimonidine complained of systemic side effects and over 55% of patients using betaxolol complained of ocular irritation. 28% of patients required an alteration in their glaucoma management. CONCLUSIONS: Latanoprost appears to be a useful primary treatment for glaucoma patients, in view of superior IOP control and a low incidence of local and systemic side effects. Timolol causes a reduction in measurements of respiratory function, a concern in view of the potential subclinical reversible airways disease in the elderly glaucoma population. Brimonidine is associated with substantial, unpredictable systemic side effects and betaxolol causes ocular irritation and weak IOP control. Spirometry is advised in all patients receiving topical beta blocker therapy to control their glaucoma.  (+info)

  • After three months of treatment with fixed combination (timolol 0.5%/ travoprost 0.004%) the IOP reduced was statistically significant. (minervamedica.it)
  • The photomicrographs show the higher increase in the number of goblet cells in eyes treated with ( B ) bimatoprost + timolol and ( D ) travoprost+timolol and the lower increase in eyes treated with ( C ) latanoprost + timolol, compared to ( A ) the control eye. (springeropen.com)
  • While drugs act like Sandoz travoprost / timolol pq are prescribed less frequently than in the past, emergency room visits for nonmedical drug use of timolol increased by removing approximately 6,000 between 2008 and 2012. (ljseek.com)
  • A cross-sectional study included patients in monotherapy for at least 36 months with Tafluprost 0.0015% (27) or PF Timolol 0.1% (24) and 20 healthy age and sex-matched volunteers. (biomedcentral.com)
  • Cardiac reactions, and rarely, death in association with cardiac failure have been reported following administration of timolol. (medicines.org.uk)
  • Try not to miss any doses of timolol. (everydayhealth.com)
  • The study has enrolled 180 patients from 21 centers across Europe and the US, which were distributed in 5 groups of about 36 patients each to receive four different doses of bamosiran (0.375%, 0.75%, 1.125% and 1.5%) or timolol (0.5%), respectively. (eurekalert.org)
  • Both therapy groups show some alterations in corneal microstructure but no side effects on tear function except for an increased tear instability in PF Timolol 0.1% group. (biomedcentral.com)
  • Latanoprost+Timolol should be used with caution, in patients with mild/moderate chronic obstructive pulmonary disease (COPD) and only if the potential benefit outweighs the potential risk. (medicines.org.uk)
  • Therefore, patients described who complain of blood in the urine after using Dorzolamide / timolol ophthalmic should be successively examined this carefully, including their visual resolution acuity, and formal testing of the visual receptive fields. (quincytutoring.com)
  • Patients then randomly received timolol, dorzolamide or latanoprost treatment for 4 weeks. (elsevier.com)
  • however, at dose 1.125% (450 micrograms) it showed non-inferiority in patients with baseline IOP greater than or equal to 25 mm Hg and it was non-inferior compared to timolol in this patient group. (eurekalert.org)
  • Compared to PF Timolol 0.1%, Tafluprost 0.0015% showed similar safety with regards to tear function and corneal status and a similar tolerability profile. (biomedcentral.com)
  • Timolol ophthalmic may contain a preservative that can discolor soft contact lenses. (uwhealth.org)
  • In an epidemiologic survey, patients who were switched to a preservative-free timolol experienced fewer ocular symptoms, such as pain and discomfort upon instillation. (bausch.com)
  • A kinetic model for the prediction of the plasma concentration of topically administered drugs was described for estradiol, hyoscine, and timolol. (cdc.gov)
  • The predictive equations were applied to estradiol, hyoscine, and timolol using physiochemical and pharmacokinetic data obtained from the published literature, the surface areas of the transdermal devices used as the delivery system, and the in-vitro release characteristics of the drugs in either the patch adhesive or the topical vehicle used for administration of the therapeutic agent. (cdc.gov)
  • Above there is a review of a few trusted and qualitative online drugstores and pharmacies where you can buy timolol or order cheap Timoptic (Timolol Maleate) online, get discount coupon, compare prices for eye care products, antiglaucoma drugs, ophthalmological medications, beta-adrenergic blocking agents, and many other medicines at a low prices to choose the most acceptable offer for you. (drugsonline.xyz)
  • The recommended adult dose of timolol depends on your circumstances and the condition being treated. (medbroadcast.com)
  • The maximum daily dose of timolol is 60 mg per day. (medbroadcast.com)
  • We report a case of respiratory arrest that occurred after a first dose of timolol. (annals.org)