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Paul Samsonov
Paul Samsonov

Beta-adrenergic Blocking Agent

Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline.

beta-adrenergic blocking agent

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The aim of this study was to evaluate the pharmacokinetic variability of beta-adrenergic blocking agents used in cardiology by reviewing single-dose and steady-state pharmacokinetic studies from the literature. PubMed was searched for pharmacokinetic studies of beta-adrenergic blocking agents, both single-dose and steady-state studies. The studies included reported maximum plasma concentration (Cmax) and/or area under the concentration curve (AUC). The coefficient of variation (CV%) was calculated for all studies, and a CV% 40% was considered high variability. The Cmax and AUC were reported a total of 672 times in 192 papers. Based on AUC, metoprolol, propranolol, carvedilol, and nebivolol showed high pharmacokinetic variability (highest first), whereas bisoprolol, atenolol, sotalol, labetalol, nadolol, and pindolol showed low to moderate variability (lowest first). We have shown a high interindividual pharmacokinetic variability that varies markedly in different beta-adrenergic blocking agents; the extreme being steady state ratios as high as 30 in metoprolol. A more personalized approach to the medical treatment of patients may be obtained by combining known pharmacokinetic information about variability, pharmaco-genetics and -dynamics, and patient characteristics, to avoid adverse events or lack of treatment effect.

Beta-blockers are some of the most frequently used medications in medicine and are usually well tolerated. Common side effects are those that are caused by the beta-adrenergic blockade and include bradycardia, fatigue, dizziness, depression, memory loss, insomnia, impotence, cold limbs and, less commonly, severe hypotension, heart failure and acute bronchospasm. Beta-blockers have been associated with a minimally increased rate of serum aminotransferase elevations and have rarely been associated with clinically apparent liver injury. Isolated case reports of idiosyncratic hepatotoxicity due to beta-blockers have been published, but there have been few case series. The case reports that have been published provide a general pattern of injury with a typical time to onset of 2 to 24 weeks and a hepatocellular pattern of serum enzyme elevations. Most cases have been mild and self-limiting, but fatal cases have been reported. Switching from one beta-blocker to another has not always resulted in recurrence of liver injury, although there have been only rare reports of such cross challenges. Most information on hepatotoxicity is available on the commonly used beta-blockers which include (and the number of prescriptions filled in 2007 for each): atenolol (42 million), metoprolol (27 million), propranolol (6.1 million), bisoprolol (4.3 million), carvedilol (2.9 million), labetalol (2.6 million), and nadolol (1.8 million). Labetalol and acebutolol have been associated with the most numbers of published cases (likelihood scores "C"), which is particularly striking in view of their relative frequency of use. Rare cases have been linked to atenolol, carvedilol and metoprolol therapy (likelihood scores "D").

Objectives: This analysis was performed to assess whether beta-adrenergic blocking agent use is associated with reduced mortality in the Studies of Left Ventricular Dysfunction (SOLVD) and to determine if this relationship is altered by angiotensin-converting enzyme (ACE) inhibitor use.

Results: The 1,015 (24%) Prevention trial patients and 197 (8%) Treatment trial patients receiving beta-blockers had fewer symptoms, higher ejection fractions and different use of medications than patients not receiving beta-blockers. On univariate analysis, beta-blocker use was associated with significantly lower mortality than nonuse in both trials. Moreover, a synergistic reduction in mortality with use of both a beta-blocker and enalapril was suggested in the Prevention trial. After adjusting for important prognostic variables with Cox multivariate analysis, the association of beta-adrenergic blocking agent use with reduced mortality remained significant for Prevention trial patients receiving enalapril. Lower rates of arrhythmic and pump failure death and risk of death or hospitalization for heart failure were observed.

The chemistry, pharmacology, pharmacokinetics, hemodynamic and electrophysiologic effects, clinical efficacy, adverse effects, drug interactions, compatibility and stability, dosage, and administration of esmolol hydrochloride are reviewed. Esmolol produces competitive blockade of beta receptors in both animals and humans. It does not possess membrane-stabilizing, intrinsic sympathomimetic, or alpha-adrenergic blocking activity. The relative cardioselectivity of esmolol is similar to that of metoprolol. Esterase metabolism accounts for the rapid total body clearance of 285 mL/kg/min and elimination half-life of 9.2 minutes. Its rapid metabolism following continuous intravenous infusion results in the rapid offset of pharmacologic effect after drug administration is discontinued. In patients with supraventricular tachyarrhythmias, esmolol produces rapid control of heart rate in an average effective dosage range from 97.2 to 115.0 micrograms/kg/min and effects that are similar to propranolol. Esmolol is effective and safe in managing tachycardia and hypertension during surgical stress and may be useful in postoperative hypertension or elevated heart rates during myocardial ischemia. Esmolol does not appear to interact with digoxin, morphine, warfarin, or succinylcholine to any clinically important extent. The most frequent adverse effects associated with esmolol infusion are hypotension and phlebitis. Hypotension can be avoided by careful titration, and if encountered, it can be rapidly resolved by dosage adjustment or discontinuation of the infusion. The ultrashort half-life and duration of action of esmolol may allow safer application of beta blockade in critically ill patients.

Beta blockers, also called beta adrenergic blocking agents, block the release of the stress hormones adrenaline and noradrenaline in certain parts of the body. This results in a slowing of the heart rate and reduces the force at which blood is pumped around your body.

Beta blockers are classified as being non-selective and selective. Non-selective beta blockers, such as propranolol, are active in blocking adrenaline and noradrenaline in other areas of the body, as well as the heart.

Beta-adrenergic blocking agents (or beta-blockers) have been frequently used to treat various cardiovascular disorders such as hypertension, ischemic heart disease, cardiac arrhythmias, and congestive heart failure1,2,3,4. Clinicians often refrain from prescribing them for patients with an underlying disease of concern to adverse events, such as asthma, diabetes mellitus, and peripheral artery disease5. In fact, acute bronchoconstriction with leading asthma exacerbation is the most crucial side effect of beta-blockers, for which several review articles and practice guidelines have advised avoiding the use of beta-blockers in patients with asthma6,7,8,9. Furthermore, beta-blockers are one of the first-line treatment agents for thyrotoxicosis10 and essential tremor11, as well as for preventing variceal bleeding in patients with portal hypertension12 and aortic aneurysm in Marfan syndrome13. Although there is considerable evidence for the effectiveness and benefits of beta-blockers in treating these diseases, the associated adverse events such as an asthma attack create a dilemma for physicians considering treatment with beta-blockers for patients with asthma.

The network structure of (A) individual beta-blocking agents among the overall participants and (B) individual beta-blocking agents among participants with a baseline history of asthma. The lines between nodes represent direct comparisons in various trials, and the size of each circle is proportional to the size of the population involved in each specific treatment. The thickness of the lines is proportional to the number of trials connected to the network. Ace oral acebutolol, Ate oral atenolol, Bev oral bevantolol, Bis oral bisoprolol, Car oral carvedilol, Cat oral carteolol, Cel oral celiprolol, CI confidence interval, CPro oral celiprolol and propranolol, iEsm infusion of esmolol, iPac infusion of practolol, iPLab infusion of propranolol and labetalol, iPro infusion of propranolol, iSot infusion of sotalol, iTol infusion of tolamolol, Lab oral dilevalol or oral labetalol, Met oral metoprolol, Nad oral nadolol, Oxp oral oxprenolol, Pin oral pindolol, Pla Placebo/control, Pra oral practolol, Pro oral propranolol, Sot oral sotalol, Tim oral timolol.

Background: Grapefruit juice was recently found to decrease plasma concentrations of the beta-adrenergic receptor-blocking agent celiprolol. Our objective was to investigate the effect of orange juice on the pharmacokinetics of celiprolol in healthy subjects.

Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the sympathetic nervous system[1] in the body. The sympathetic nervous system(SNS) is an autonomic nervous system that we cannot control by will. It triggers a series of responses after the body releases chemicals named noradrenaline and epinephrine.[1] These chemicals will act on adrenergic receptors, with subtypes Alpha-1, Alpha-2, Beta-1, Beta-2, Beta-3, which ultimately allow the body to trigger a "fight-or-flight" response to handle external stress.[1] These responses include vessel constriction in general vessels whereas there is vasodilation in vessels that supply skeletal muscles or in coronary vessels.[1] Additionally, the heart rate and contractile force increase when SNS is activated, which may be harmful to cardiac function as it increases metabolic demand.[1] 041b061a72


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