Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.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.Adrenergic beta-1 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Betaxolol: A cardioselective beta-1-adrenergic antagonist with no partial agonist activity.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.Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638)Double-Blind Method: A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.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: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Bendroflumethiazide: A thiazide diuretic with actions and uses similar to those of HYDROCHLOROTHIAZIDE. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810)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.Celiprolol: A cardioselective beta-1 adrenergic antagonist that has intrinsic symopathomimetic activity. It is used in the management of ANGINA PECTORIS and HYPERTENSION.Oxprenolol: A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.Butoxamine: A beta-2 selective adrenergic antagonist. It is used primarily in animal and tissue experiments to characterize BETA-2 ANDRENERGIC RECEPTORS.Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.Receptors, Adrenergic, beta: One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.Clinical Trials as Topic: Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.Nadolol: A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.Drug Therapy, Combination: Therapy with two or more separate preparations given for a combined effect.Physical Exertion: Expenditure of energy during PHYSICAL ACTIVITY. Intensity of exertion may be measured by rate of OXYGEN CONSUMPTION; HEAT produced, or HEART RATE. Perceived exertion, a psychological measure of exertion, is included.Random Allocation: A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.Pulse: The rhythmical expansion and contraction of an ARTERY produced by waves of pressure caused by the ejection of BLOOD from the left ventricle of the HEART as it contracts.Receptors, Adrenergic, beta-1: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Hyperthyroidism: Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.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.Polonium: Polonium. A radioactive element that is a member of the chalcogen family. It has the atomic symbol Po, atomic number 84, and the atomic weight of the isotope with the longest half-life (209Po) is 208.98. It decays by alpha-emission.Acoustics: The branch of physics that deals with sound and sound waves. In medicine it is often applied in procedures in speech and hearing studies. With regard to the environment, it refers to the characteristics of a room, auditorium, theatre, building, etc. that determines the audibility or fidelity of sounds in it. (From Random House Unabridged Dictionary, 2d ed)Horse Diseases: Diseases of domestic and wild horses of the species Equus caballus.Pharmacists: Those persons legally qualified by education and training to engage in the practice of pharmacy.Talaromyces: A fungal genus in the family Trichocomaceae, order EUROTIALES, characterized by loose hyphal fruiting bodies containing spherical asci. Anamorphs include PENICILLIUM and PAECILOMYCES.Hypothyroidism: A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.Congenital Hypothyroidism: A condition in infancy or early childhood due to an in-utero deficiency of THYROID HORMONES that can be caused by genetic or environmental factors, such as thyroid dysgenesis or HYPOTHYROIDISM in infants of mothers treated with THIOURACIL during pregnancy. Endemic cretinism is the result of iodine deficiency. Clinical symptoms include severe MENTAL RETARDATION, impaired skeletal development, short stature, and MYXEDEMA.Judgment: The process of discovering or asserting an objective or intrinsic relation between two objects or concepts; a faculty or power that enables a person to make judgments; the process of bringing to light and asserting the implicit meaning of a concept; a critical evaluation of a person or situation.Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.Physicians: Individuals licensed to practice medicine.Thyrotropin: A glycoprotein hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Thyrotropin stimulates THYROID GLAND by increasing the iodide transport, synthesis and release of thyroid hormones (THYROXINE and TRIIODOTHYRONINE). Thyrotropin consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the pituitary glycoprotein hormones (TSH; LUTEINIZING HORMONE and FSH), but the beta subunit is unique and confers its biological specificity.Postural Orthostatic Tachycardia Syndrome: A syndrome of ORTHOSTATIC INTOLERANCE combined with excessive upright TACHYCARDIA, and usually without associated ORTHOSTATIC HYPOTENSION. All variants have in common an excessively reduced venous return to the heart (central HYPOVOLEMIA) while upright.Tachycardia: Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.Mitral Valve Prolapse: Abnormal protrusion or billowing of one or both of the leaflets of MITRAL VALVE into the LEFT ATRIUM during SYSTOLE. This allows the backflow of blood into left atrium leading to MITRAL VALVE INSUFFICIENCY; SYSTOLIC MURMURS; or CARDIAC ARRHYTHMIA.Prolapse: The protrusion of an organ or part of an organ into a natural or artificial orifice.Mitral Valve: The valve between the left atrium and left ventricle of the heart.Mitral Valve Insufficiency: Backflow of blood from the LEFT VENTRICLE into the LEFT ATRIUM due to imperfect closure of the MITRAL VALVE. This can lead to mitral valve regurgitation.

Stroke volume decline during prolonged exercise is influenced by the increase in heart rate. (1/763)

This study determined whether the decline in stroke volume (SV) during prolonged exercise is related to an increase in heart rate (HR) and/or an increase in cutaneous blood flow (CBF). Seven active men cycled for 60 min at approximately 57% peak O2 uptake in a neutral environment (i.e., 27 degrees C, <40% relative humidity). They received a placebo control (CON) or a small oral dose (i.e., approximately 7 mg) of the beta1-adrenoceptor blocker atenolol (BB) at the onset of exercise. At 15 min, HR and SV were similar during CON and BB. From 15 to 55 min during CON, a 13% decline in SV was associated with an 11% increase in HR and not with an increase in CBF. CBF increased mainly from 5 to 15 min and remained stable from 20 to 60 min of exercise in both treatments. However, from 15 to 55 min during BB, when the increase in HR was prevented by atenolol, the decline in SV was also prevented, despite a normal CBF response (i.e., similar to CON). Cardiac output was similar in both treatments and stable throughout the exercise bouts. We conclude that during prolonged exercise in a neutral environment the decline in SV is related to the increase in HR and is not affected by CBF.  (+info)

ACE inhibitor versus beta-blocker for the treatment of hypertension in renal allograft recipients. (2/763)

Angiotensin-converting enzyme (ACE) inhibitors have been shown to slow the progression of chronic renal failure. However, the value of ACE inhibitors for the treatment of hypertension in renal allograft recipients has not been established. ACE inhibitors dilate the efferent glomerular arteriole, an effect that may aggravate the decrease in glomerular filtration rate resulting from cyclosporine-induced vasoconstriction at the afferent glomerular arteriole. Therefore, the goal of this double-blind, randomized study was to compare the antihypertensive and renal effects of the ACE inhibitor quinapril with those of the beta-blocker atenolol in renal allograft recipients in whom hypertension developed 6 to 12 weeks after transplantation. All patients received cyclosporine as an immunosuppressant and had stable graft function (serum creatinine concentration, <220 micromol/L) at entry into the study. Twenty-nine patients who received quinapril (daily dose titrated between 2.5 and 20 mg) and 30 patients who received atenolol (daily dose titrated between 12.5 and 100 mg) completed the 24-month study. The two groups did not differ in age, sex ratio, height, and weight before entry into the study. Quinapril decreased diastolic blood pressure from 96+/-1 to 84+/-1 mm Hg (average throughout treatment period), and atenolol decreased diastolic blood pressure from 96+/-1 to 83+/-1 mm Hg. The serum creatinine concentration did not change significantly in either group after 24 months (129+/-8 micromol/L at entry and 148+/-19 micromol/L after 24 months in the quinapril group and 131+/-6 micromol/L at entry and 152+/-15 micromol/L after 24 months in the atenolol group; P=NS for both groups). After 24 months, the change in urinary albumin excretion from baseline was -10+/-15 mg/d in the quinapril group and 52+/-32 mg/d in the atenolol group (P=0.03). These results show that quinapril and atenolol are effective antihypertensive drugs when used after renal transplantation. Moreover, compared with atenolol, quinapril has no adverse effects on graft function. The relative reduction in albuminuria observed with quinapril as compared with atenolol could indicate a beneficial effect of quinapril on long-term graft function.  (+info)

Comparison of atenolol with propranolol in the treatment of angina pectoris with special reference to once daily administration of atenolol. (3/763)

Fourteen patients with angina pectoris completed a double blind trial of atenolol 25 mg, 50 mg, and 100 mg twice daily and propranolol 80 mg thrice daily. In comparison with placebo, all active treatments significantly reduced anginal attacks, consumption of glyceryl trinitrate, resting and exercise heart rate, resting and exercise systolic blood pressure, and significantly prolonged exercise time. There was no significant difference between the effects of propranolol and atenolol. Nine patients completed a further trial comparing atenolol given once or twice daily. Both regimens were effective and there was no significant difference between the reductions in anginal attacks, glyceryl trinitrate consumption, systolic blood pressure, or heart rate. Twenty-four-hour ambulatory electrocardiograms showed that atenolol consistently reduced heart rate throughout the 24-hour period whether given once or twice daily. Atenolol is a potent antianginal agent which, in most patients, is likely to be effective once daily.  (+info)

Bradykinin B1 and B2 receptors, tumour necrosis factor alpha and inflammatory hyperalgesia. (4/763)

The effects of BK agonists and antagonists, and other hyperalgesic/antihyperalgesic drugs were measured (3 h after injection of hyperalgesic drugs) in a model of mechanical hyperalgesia (the end-point of which was indicated by a brief apnoea, the retraction of the head and forepaws, and muscular tremor). DALBK inhibited responses to carrageenin, bradykinin, DABK, and kallidin. Responses to kallidin and DABK were inhibited by indomethacin or atenolol and abolished by the combination of indomethacin + atenolol. DALBK or HOE 140, given 30 min before, but not 2 h after, carrageenin, BK, DABK and kallidin reduced hyperalgesic responses to these agents. A small dose of DABK+ a small dose of BK evoked a response similar to the response to a much larger dose of DABK or BK, given alone. Responses to BK were antagonized by HOE 140 whereas DALBK antagonized only responses to larger doses of BK. The combination of a small dose of DALBK with a small dose of HOE 140 abolished the response to BK. The hyperalgesic response to LPS (1 microg) was inhibited by DALBK or HOE 140 and abolished by DALBK + HOE 140. The hyperalgesic response to LPS (5 microg) was not antagonized by DALBK + HOE 140. These data suggest: (a) a predominant role for B2 receptors in mediating hyperalgesic responses to BK and to drugs that stimulate BK release, and (b) activation of the hyperalgesic cytokine cascade independently of both B1 and B2 receptors if the hyperalgesic stimulus is of sufficient magnitude.  (+info)

Actions of vasoactive intestinal peptide on the rat adrenal zona glomerulosa. (5/763)

Previous studies, by this group and others, have shown that vasoactive intestinal peptide (VIP) stimulates aldosterone secretion, and that the actions of VIP on aldosterone secretion by the rat adrenal cortex are blocked by beta adrenergic antagonists, suggesting that VIP may act by the local release of catecholamines. The present studies were designed to test this hypothesis further, by measuring catecholamine release by adrenal capsular tissue in response to VIP stimulation. Using intact capsular tissue it was found that VIP caused a dose-dependent increase in aldosterone secretion, with a concomitant increase in both adrenaline and noradrenaline release. The effects of VIP on aldosterone secretion were inhibited by atenolol, a beta1 adrenergic antagonist, but not by ICI-118,551, a beta2 adrenergic antagonist. Binding studies were carried out to investigate VIP receptors. It was found that adrenal zona glomerulosa tissue from control rats contained specific VIP binding sites (Bmax 853+/-101 fmol/mg protein; Kd 2.26+/-0.45 nmol/l). VIP binding was not displaced by ACTH, angiotensin II or by either of the beta adrenergic antagonists. The response to VIP in adrenals obtained from rats fed a low sodium diet was also investigated. Previous studies have found that adrenals from animals on a low sodium diet exhibit increased responsiveness to VIP. Specific VIP binding sites were identified, although the concentration or affinity of binding sites in the low sodium group was not significantly different from the controls. In the low sodium group VIP was found to increase catecholamine release to the same extent as in the control group, however, in contrast to the control group, the adrenal response to VIP was not altered by adrenergic antagonists in the low sodium group. These data provide strong support for the hypothesis that VIP acts by the local release of catecholamines in adrenal zona glomerulosa tissue in normal animals. It does not appear that VIP acts through the same mechanism in animals maintained on a low sodium diet. The mechanism by which VIP stimulates aldosterone in this group remains to be determined.  (+info)

Supervised atenolol therapy in the management of hemodialysis hypertension. (6/763)

BACKGROUND: Uncontrolled hypertension continues to be a common problem, particularly in noncompliant hemodialysis patients. Atenolol, a water soluble beta-blocker has a prolonged half-life in renal failure and may serve as a useful antihypertensive agent in these patients. METHODS: Hypertension was diagnosed by ambulatory blood pressure monitoring for 44 hours during an interdialytic interval in eight chronic hemodialysis patients receiving no antihypertensive therapy. An average daytime blood pressure greater than 140/90 mm Hg or an average nighttime blood pressure greater than 120/80 mm Hg was used to define uncontrolled hypertension. Patients were then administered atenolol (25 mg) following hemodialysis three times a week. The efficacy of therapy was judged by ambulatory blood pressure monitoring three weeks after instituting atenolol therapy. Blood pressure loads above the threshold blood pressures during the day or night were also calculated and compared before and after three weeks of atenolol therapy. RESULTS: The mean 44-hour ambulatory blood pressure (ABP) fell from 144 +/- 14/80 +/- 7 mm Hg to 127 +/- 13/69 +/- 10 mm Hg (P < 0.001). The heart rate fell from 85 +/- 11 to 70 +/- 11 beats per minute. The systolic and diastolic blood pressure load was reduced from 71 +/- 25% and 30 +/- 24% to 35 +/- 26% and 11 +/- 17%, respectively (P < 0.001). There was a persistent antihypertensive effect over 44 hours. The blood pressure reduction was achieved without any increase in intradialytic symptomatic or asymptomatic hypotensive episodes, reduction in delivered dialysis, or statistically significant changes in serum potassium or glucose. CONCLUSIONS: A supervised administration of atenolol following hemodialysis effectively and safely controls hypertension in chronic hemodialysis patients. This therapy can be particularly valuable for noncompliant hemodialysis patients.  (+info)

Thermogenic effects of sibutramine and its metabolites. (7/763)

1. The thermogenic activity of the serotonin and noradrenaline reuptake inhibitor sibutramine (BTS 54524; Reductil) was investigated by measuring oxygen consumption (VO2) in rats treated with sibutramine or its two pharmacologically-active metabolites. 2. Sibutramine caused a dose-dependent rise in VO2, with a dose of 10 mg kg(-1) of sibutramine or its metabolites producing increases of up to 30% that were sustained for at least 6 h, and accompanied by significant increases (0.5-1.0 degrees C) in body temperature. 3. Based on the accumulation in vivo of radiolabelled 2-deoxy-[3H]-glucose, sibutramine had little or no effect on glucose utilization in most tissues, but caused an 18 fold increase in brown adipose tissue (BAT). 4. Combined high, non-selective doses (20 mg kg(-1)) of the beta-adrenoceptor antagonists, atenolol and ICI 118551, inhibited completely the VO2 response to sibutramine, but the response was unaffected by low, beta1-adrenoceptor-selective (atenolol) or beta2-adrenoceptor-selective (ICI 118551) doses (1 mg kg(-1)). 5. The ganglionic blocking agent, chlorisondamine (15 mg kg(-1)), inhibited completely the VO2 response to the metabolites of sibutramine, but had no effect on the thermogenic response to the beta3-adrenoceptor-selective agonist BRL 35135. 6. Similar thermogenic responses were produced by simultaneous injection of nisoxetine and fluoxetine at doses (30 mg kg(-1)) that had no effect on VO2 when injected individually. 7. It is concluded that stimulation of thermogenesis by sibutramine requires central reuptake inhibition of both serotonin and noradrenaline, resulting in increased efferent sympathetic activation of BAT thermogenesis via beta3-adrenoceptor, and that this contributes to the compound's activity as an anti-obesity agent.  (+info)

Inotropic and sympathetic responses to the intracoronary infusion of a beta2-receptor agonist: a human in vivo study. (8/763)

BACKGROUND: On the basis of the presence of beta2-receptors within the sympathetic nervous system, beta2-stimulation may increase cardiac sympathetic outflow. We addressed the hypothesis that sympathoexcitatory beta2-receptors are present in the human left ventricle. METHODS AND RESULTS: The beta2-agonist salbutamol was infused into the left coronary artery in 3 groups of patients: group 1 (n=9, no beta-blocker therapy), group 2 (n=7, beta1-selective blockade with atenolol), and group 3 (n=6, nonselective beta-blockade with nadolol). Left ventricular +dP/dt in response to increasing concentrations of salbutamol was measured in all groups, and cardiac norepinephrine spillover was measured in group 1. There were no systemic hemodynamic changes in any group. Salbutamol resulted in a 44+/-6% increase in +dP/dt in group 1, a 25+/-6% increase in group 2 (P<0.05 versus group 1), and no increase in group 3. Salbutamol also resulted in a 124+/-37% increase in cardiac norepinephrine spillover in group 1 (P<0.05). CONCLUSIONS: Evidence that salbutamol increased norepinephrine release from cardiac sympathetic nerves was provided by the observations that atenolol suppressed the salbutamol inotropic response, demonstrating that this response was mediated in part by beta1-receptors and that salbutamol also resulted in an increase in cardiac norepinephrine spillover. This result provides in vivo evidence, in humans, for the role of sympathoexcitatory cardiac beta2-receptors.  (+info)

  • While it was originally thought and promoted that atenolol can be used once a day for isolated hypertension because the central nervous system pharmacodynamic effect persists longer, subsequent studies suggest atenolol should be dosed twice a day even for hypertension. (
  • Atenolol is commonly used to treat hypertension . (
  • Atenolol 50mg may be prescribed to you with or without other medications to treat high blood pressure (hypertension). (
  • I Losartan Intervension for Endpoint Reduction in Hypertension (LIFE) studien (n = 9 193 individer) var blodtrykksreduksjonen etter 4 år identisk hos pasienter behandlet med AII-reseptorblokkeren losartan og atenolol (7). (
  • Twenty patients with mild or moderate essential hypertension participated in a double-blind crossover randomized trial aimed at assessing, by echocardiography, the hemodynamic effects of the antihypertensive therapy with atenolol administered once daily (100 mg) alone or combined with chlortalidone (25 mg) in fixed combination. (
  • Atenolol requires a prescription from your veterinarian. (
  • Tell your veterinarian if your pet is being given any prescription or over-the-counter medicines, as they may interact with Atenolol. (
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  • This preferential effect is not absolute, however, and at higher doses, atenolol inhibits beta 2 - adrenoreceptors, chiefly located in the bronchial and vascular musculature. (
  • hydrochlorothiazide atenolol.hypoglycemia and atenolol.overdose atenolol.atenolol.atenolol picture.fosinopril and atenolol.atenolol.atenolol 50 mg 99 z identification.atenolol effects on pregnancy.biowaiver of atenolol.i take metoprolol and atenolol.atenolol and diabetics.atenolol drug interaction.atenolol for forom on atenolol.atenolol breastfeeding. (
  • Atenolol is a beta 1 -selective (cardioselective) beta-adrenergic receptor blocking agent without membrane stabilizing or intrinsic sympathomimetic (partial agonist) activities. (
  • In medicine , atenolol is a cardioselective adrenergic beta-antagonist that is "possessing properties and potency similar to propranolol , but without a negative inotropic effect. (
  • Unlike propranolol or metoprolol, but like nadolol, atenolol undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion. (
  • Atenolol also differs from propranolol in that only a small amount (6% to 16%) is bound to proteins in the plasma. (
  • Cimetidine, a P-450 enzyme inhibitor, increases the systemic bioavailability of propranolol and labetalol, which undergo extensive metabolism, but does not affect the clearance of Atenolol, which is excreted largely unchanged. (
  • I en meta-analyse av 31 randomiserte, placebokontrollerte studier hos pasienter med et gjennomgått hjerteinfarkt (n = 24 974), reduserte timolol, metoprolol og propranolol etter 6-48 måneder statistisk signifikant risikoen for død med henholdsvis 41 %, 20 % og 29 % (5). (
  • After training the maximal heart rate did not change in the placebo group, while treatment with propranolol and atenolol reduced at 24.6 and 21.9%, respectively. (
  • The groups treated with propranolol and atenolol were also similarly decreased. (
  • The use of propranolol or atenolol had no additional significant effect on natural killer cell activity. (
  • The groups given atenolol or propranolol tended to increase somewhat more than the placebo group, although this differnece was not statistically significant. (
  • The number of mature T-lymphocytes measured by the E-rosetting technique increased significantly consequent to physical conditioning, with propranolol and/or atenolol having no additional effect. (
  • Freund, B. J. / Modification of cellular immune functions in humans by endurance exercise training during β-adrenergic blockade with atenolol or propranolol . (
  • In this study atenolol had similar outcomes to other antihypertensive agents . (
  • These results suggest that the association of chlortalidone potentiates the antihypertensive effect of atenolol by acting through a different mechanism. (
  • Ricciardelli, B, Cuocolo, A & De Luca, N 1985, ' Hemodynamic effects of the antihypertensive treatment with atenolol plus chlortalidone in fixed combination: A double-blind crossover comparison with atenolol ', Current Therapeutic Research , vol. 37, no. 5, pp. 901-911. (
  • Atenolol may be prescribed by your healthcare professional for treating irregular heartbeats, heart failure, prevention of migraine headaches, and alcohol withdrawal symptoms. (
  • I en meta-analyse (fire studier, 6 825 pasienter fulgt i gjennomsnitt i 4,6 år) fant Carlberg og medarbeidere at atenolol reduserte et forhøyet blodtrykk i forhold til placebo eller ingen behandling (8). (
  • After a baseline evaluation (time 0), patients were randomly assigned to a placebo (group 1) or atenolol (group 2) therapy. (
  • Do not stop giving atenolol abruptly unless you are directed to do so by your veterinarian. (
  • Atenolol for acute myocardial infarction - meta-analysis of atenolol subgroup from larger meta-analysis by Brandler. (
  • A significant beta-blocking effect of atenolol, as measured by reduction of exercise tachycardia, is apparent within one hour following oral administration of a single dose. (