Beta blockers (sometimes written as β-blocker) is a class of drugs A pharmaceutical drug, also referred to as medicine, medication or medicament, can be loosely defined as any chemical substance intended for use in the medical diagnosis, cure, treatment, or prevention of disease used for various indications, but particularly for the management of cardiac arrhythmias Cardiac dysrhythmia is a term for any of a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart. The heart beat may be too fast or too slow, and may be regular or irregular, cardioprotection after myocardial infarction Myocardial infarction or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of (heart attack), and hypertension Hypertension or high blood pressure is a chronic medical condition in which the systemic arterial blood pressure is elevated. It is the opposite of hypotension. It is classified as either primary (essential) or secondary. About 90–95% of cases are termed "primary hypertension", which refers to high blood pressure for which no medical. As beta adrenergic The adrenergic receptors are a class of G protein-coupled receptors that are targets of the catecholamines, especially noradrenaline (norepinephrine) and adrenaline (epinephrine). Although dopamine is a catecholamine, its receptors are in a different category receptor antagonists A receptor antagonist is a type of receptor ligand or drug that does not provoke a biological response itself upon binding to a receptor, but blocks or dampens agonist-mediated responses. In pharmacology, antagonists have affinity but no efficacy for their cognate receptors, and binding will disrupt the interaction and inhibit the function of an, they diminish the effects of epinephrine Epinephrine is a hormone and neurotransmitter.. It increases heart rate, contracts blood vessels, dilates air passages and participates in the fight-or-flight response of the sympathetic nervous system. Chemically, epinephrine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenylalanine and tyrosine (adrenaline) and other stress hormones. Invented by Sir James W. Black Sir James Whyte Black, OM, FRS, FRSE, FRCP is a Scottish doctor and pharmacologist who invented Propranolol, synthesized Cimetidine and was awarded the Nobel Prize for Medicine in 1988 for these discoveries in the late 1950s, Propranolol US FDA:link was the first clinically useful beta blocker; it revolutionized the medical management of angina pectoris Angina pectoris, commonly known as angina, is severe chest pain due to ischemia of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Latin angina (" and is considered to be one of the most important contributions to clinical medicine and pharmacology Pharmacology is the branch of biology concerned with the study of drug action. More specifically, it is the study of the interactions that occur between a living organism and chemicals that affect normal or abnormal biochemical function. If substances have medicinal properties, they are considered pharmaceuticals. The field encompasses drug of the 20th century.[1] Beta blockers may also be referred to as beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists.
Beta blockers block the action of endogenous Endogenous substances are those that originate from within an organism, tissue, or cell . Endogenous retroviruses are caused by ancient infections of germ cells in humans, mammals and other vertebrates. Their proviruses remain in the genome and are passed on to the next generation catecholamines Catecholamines are sympathomimetic "fight-or-flight" hormones released by the adrenal glands in response to stress. They are part of the sympathetic nervous system (epinephrine Epinephrine is a hormone and neurotransmitter.. It increases heart rate, contracts blood vessels, dilates air passages and participates in the fight-or-flight response of the sympathetic nervous system. Chemically, epinephrine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenylalanine and tyrosine (adrenaline) and norepinephrine Norepinephrine (abbreviated norepi or NE) or noradrenaline (BAN) (abbreviated NA or NAd) is a catecholamine with multiple roles including as a hormone and a neurotransmitter (noradrenaline) in particular), on β-adrenergic receptors The adrenergic receptors are a class of G protein-coupled receptors that are targets of the catecholamines, especially noradrenaline (norepinephrine) and adrenaline (epinephrine). Although dopamine is a catecholamine, its receptors are in a different category, part of the sympathetic nervous system The sympathetic nervous system is one of the three parts of the autonomic nervous system, along with the enteric and parasympathetic systems. Its general action is to mobilize the body's resources under stress; to induce the flight-or-fight response. It is, however, constantly active at a basal level in order to maintain homeostasis which mediates the "fight or flight" response. There are three known types of beta receptor, designated β1, β2 and β3. β1-Adrenergic receptors are located mainly in the heart and in the kidneys. β2-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-receptors are located in fat cells.
Examples of beta-blockers include: acebutolol US FDA:link, betaxolol Betaxolol is a selective beta1 receptor blocker used in the treatment of hypertension and glaucoma. Being selective for beta1 receptors, it typically has fewer systemic side effects than non-selective beta-blockers, for example, not causing bronchospasm (mediated by beta2 receptors) as timolol may. Betaxolol also shows greater affininty for beta1, bisoprolol US FDA:link, esmolol Esmolol is a cardioselective beta1 receptor blocker with rapid onset, a very short duration of action, and no significant intrinsic sympathomimetic or membrane stabilising activity at therapeutic dosages, propranolol US FDA:link, atenolol Atenolol is a selective β1 receptor antagonist, a drug belonging to the group of beta blockers (sometimes written β-blockers), a class of drugs used primarily in cardiovascular diseases. Introduced in 1976, atenolol was developed as a replacement for propranolol in the treatment of hypertension. The chemical works by slowing down the heart and, labetalol Labetalol is a mixed alpha/beta adrenergic antagonist, which is used to treat high blood pressure, carvedilol Carvedilol is a non-selective beta blocker/alpha-1 blocker indicated in the treatment of mild to moderate congestive heart failure . It is marketed under various trade names including Coreg (GSK), Dilatrend (Roche), Eucardic (Roche), and Carloc (Cipla) as a generic drug (as of September 5, 2007 in the U.S.)., and as a controlled-release, metoprolol US FDA:link, and nebivolol US FDA:link.
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β-Receptor antagonism
Stimulation of β1 receptors by epinephrine Epinephrine is a hormone and neurotransmitter.. It increases heart rate, contracts blood vessels, dilates air passages and participates in the fight-or-flight response of the sympathetic nervous system. Chemically, epinephrine is a catecholamine, a monoamine produced only by the adrenal glands from the amino acids phenylalanine and tyrosine induces a positive chronotropic Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate and inotropic An inotrope (from Greek in-, meaning fibre or sinew) is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin Renin , also known as angiotensinogenase is an enzyme that participates in the body's renin-angiotensin system (RAS) that mediates extracellular volume (i.e., that of the blood plasma, lymph and interstitial fluid), and arterial vasoconstriction. Thus, it regulates the body's mean arterial blood pressure release. Stimulation of β2 receptors induces smooth muscle Smooth muscle is an involuntary non-striated muscle. It is divided into two sub-groups; the single-unit and multiunit smooth muscle. Within single-unit smooth muscle tissues, the autonomic nervous system innervates a single cell within a sheet or bundle and the action potential is propagated by gap junctions to neighboring cells such that the relaxation, induces tremor in skeletal muscle Skeletal muscle is a form of striated muscle tissue existing under control of the somatic nervous system. It is one of three major muscle types, the others being cardiac and smooth muscle. As its name suggests, most skeletal muscle is attached to bones by bundles of collagen fibers known as tendons, and increases glycogenolysis Glycogenolysis is the conversion of glycogen polymers to glucose monomers. Glycogen is catabolized by removal of a glucose monomer through cleavage with inorganic phosphate to produce glucose-1-phosphate. This derivative of glucose is then converted to glucose-6-phosphate, an intermediate in glycolysis in the liver The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxification, protein synthesis, and production of biochemicals necessary for digestion. The liver is necessary for survival; there is currently no way to compensate for the absence of liver function and skeletal muscle Skeletal muscle is a form of striated muscle tissue existing under control of the somatic nervous system. It is one of three major muscle types, the others being cardiac and smooth muscle. As its name suggests, most skeletal muscle is attached to bones by bundles of collagen fibers known as tendons. Stimulation of β3 receptors induces lipolysis Lipolysis is the hydrolysis of lipids. Metabolically it is the breakdown of triglycerides into free fatty acids within cells. When fats are broken down for energy the process is known as beta oxidation. Ketones are produced, and are found in large quantities in ketosis . Lipolysis testing strips such as Ketostix are used to recognize ketosis.
Beta blockers inhibit these normal epinephrine-mediated sympathetic The sympathetic nervous system is one of the three parts of the autonomic nervous system, along with the enteric and parasympathetic systems. Its general action is to mobilize the body's resources under stress; to induce the flight-or-fight response. It is, however, constantly active at a basal level in order to maintain homeostasis actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction, dilation of blood vessels and opening of bronchi, and also reduce tremor and breakdown of glycogen Glycogen is the molecule that functions as the secondary long-term energy storage in animal and fungi cells. It is made primarily by the liver and the muscles, but can also be made by glycogenesis within the brain and stomach. Glycogen is the analogue of starch, a less branched glucose polymer in plants, and is commonly referred to as animal.
It is therefore expected that non-selective beta blockers have an antihypertensive The antihypertensives are a class of drugs that are used to treat hypertension . Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease. There are many classes of effect. The antihypertensive mechanism appears to involve reduction in cardiac output (due to negative chronotropic and inotropic effects), reduction in renin Renin , also known as angiotensinogenase is an enzyme that participates in the body's renin-angiotensin system (RAS) that mediates extracellular volume (i.e., that of the blood plasma, lymph and interstitial fluid), and arterial vasoconstriction. Thus, it regulates the body's mean arterial blood pressure release from the kidneys, and a central nervous system The central nervous system is the part of the nervous system that coordinates the activity of all parts of the bodies of bilaterian animals—that is, all multicellular animals except sponges and radially symmetric animals such as jellyfish. It contains the majority of the nervous system and consists of the brain and the spinal cord, as well as effect to reduce sympathetic The sympathetic nervous system is one of the three parts of the autonomic nervous system, along with the enteric and parasympathetic systems. Its general action is to mobilize the body's resources under stress; to induce the flight-or-fight response. It is, however, constantly active at a basal level in order to maintain homeostasis activity (for those β-blockers that do cross the blood-brain barrier, e.g. Propranolol).
Antianginal effects result from negative chronotropic Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate and inotropic An inotrope (from Greek in-, meaning fibre or sinew) is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction effects, which decrease cardiac workload and oxygen demand. Negative chronotropic Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate properties of beta blockers allow the lifesaving property of heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states.
The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node The sinoatrial node is the impulse-generating (pacemaker) tissue located in the right atrium of the heart, and thus the generator of sinus rhythm. It is a group of cells positioned on the wall of the right atrium, near the entrance of the superior vena cava. These cells are modified cardiac myocytes. Though they possess some contractile filaments, function and atrioventricular node The atrioventricular node is a part of electrical control system of the heart that co-ordinates heart rate. It electrically connects atrial and ventricular chambers. The AV node is an area of specialized tissue between the atria and the ventricles of the heart, specifically in the posteroinferior region of the interatrial septum near the opening conduction, and prolonged atrial In anatomy, the atrium , sometimes called auricle, refers to a chamber or space. It may be the atrium of the lateral ventricle in the brain or the blood collection chamber of a heart. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system. In fish, the refractory periods. Sotalol Sotalol is a drug used in individuals with rhythm disturbances (cardiac arrhythmias) of the heart, and to treat hypertension in some individuals, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.
Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium and water retention.
Intrinsic sympathomimetic activity
Also referred to as intrinsic sympathomimetic effect, this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound such as norepinephrine). See partial agonist for a more general description.
Some beta blockers (e.g. oxprenolol, pindolol, penbutolol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.
Agents with ISA are not used in post-myocardial infarction as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia.[2]
α1-Receptor antagonism
Some beta blocker (e.g. labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.
Other effects
Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbance caused by some agents.[3]
Beta blockers protect against social anxiety: "Improvement of physical symptoms has been demonstrated with beta-blockers such as propranolol; however, these effects are limited to the social anxiety experienced in performance situations." (example: an inexperienced symphony soloist) [4]
Beta blockers can impair the relaxation of bronchial muscle (mediated by beta-2) and so should be avoided by asthmatics.
They can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor secretion.[5]
Clinical use
Large differences exist in the pharmacology of agents within the class, thus not all beta blockers are used for all indications listed below.
Indications for beta blockers include:
- Angina pectoris
- Atrial fibrillation
- Cardiac arrhythmia
- Congestive heart failure
- Essential tremor
- Glaucoma
- Hypertension
- Migraine prophylaxis
- Mitral valve prolapse
- Myocardial infarction
- Phaeochromocytoma, in conjunction with α-blocker
- Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
Beta blockers have also been used in the following conditions:
- Acute aortic dissection
- Hypertrophic obstructive cardiomyopathy
- Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications)
- Prevention of variceal bleeding in portal hypertension
- Possible mitigation of hyperhidrosis
- Social anxiety disorder and other anxiety disorders
Congestive heart failure
Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition, studies in the late 1990s showed their positive effects on morbidity and mortality in congestive heart failure.[6] [7] [8] Bisoprolol, carvedilol and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure.
Beta blockers are primarily known for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure[citation needed]. Beta blockers, in addition to their sympatholytic B1 activity in the heart, influence the renin/angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduce the heart oxygen demand by lowering extracellular volume and increasing the oxygen carrying capacity of blood. Beta blockers sympatholytic activity reduce heart rate, thereby increasing the ejection fraction of the heart despite an initial reduction in ejection fraction.
Trials have shown that beta blockers reduce the absolute risk of death by 4.5% over a 13 month period. As well as reducing the risk of mortality, the number of hospital visits and hospitalizations were also reduced in the trials.[9]
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Wed, 23 Jun 2010 16:36:04 GMT+00:00
TheHeart.Org Other current treatments represented are aspirin (86.4% of patients), beta blockers (72.5%), ACE inhibitors (49.1%), and angiotensin-receptor blockers ...
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Wed, 14 Jul 2010 18:03:22 GM
On the hunt for particulars on what do . beta blockers. do? We dwell in a competitive environment. We expertise loads of stress in our life. We experience sleepless nights on account of the carefree living. Our thought process doesn't ...
Q. After a few years of suffering with disabling anxiety/panic disorder and almost constant tachycardia, I decided to start taking atenolol to help, and it did--a lot. My anxiety level dropped tremendously, along with my heart rate and the number of palpitations I had, and I was able to go back to work last year. About a month ago I started having panic attacks again. I had 8 in one week which was probably more than I've had in the 2 years I've taken atenolol combined. My anxiety is near constant again and I am experiencing a lot of tachycardia. Can beta blockers lose their effectiveness over time? My doctor doesn't want to increase my dosage because my blood pressure is fairly low on the drug. I am also taking ativan and it seems as if both… [cont.]
Asked by Ribbons - Mon Apr 30 22:11:23 2007 - - 6 Answers - 0 Comments
A. I'm so sorry to hear of your recent experiences. Anxiety disorders are difficult but can be managed as you have experienced. There is hope. Regarding your question about beta blocker therapy and effectiveness. A physician who has examined you and is familiar with your history can accurately answer this question. The perception maybe the prescribed beta blocker therapy has lost its effectiveness but it might be the medical disorder and prescribed therapy have reached a plateau. Many meds are prescribed and can max out on dosage limits based on physiological symptoms such as your low BP. So is it the medication or is it the body's response to the medicine? Hard to answer since every person is different and unique in the reactions… [cont.]
Answered by danielromero60 - Mon Apr 30 22:27:11 2007
