what is a beta blocker and how does it work?

Answer 1

"Beta-blockers are used to lower high blood pressure, relieve angina (chest pain), correct arrhythmias (irregular heartbeats), reduce the risk of dying after a heart attack and treat heart failure."

Answer 2

Beta Blockers are a class of drugs that block beta adrenergic substances such as adrenaline (epinephrine), a key agent in the sympathetic portionof the autonomic nervous system (involuntary). By blocking the action of sympathetic nervous system on the heart, these agents relive stress on the heart. They slow the heartbeat, lessen the force with which the heart muscle contracts, and reduce blood vessel contraction in the heart, brain and body. Beta Blockers are used to treat abnormal heart rhythms, to prevent abnormally fast heart rates, or irregular heart rhythms. Since beta blockers reduece the demand of the heart muscle for oxygen, they can be useful in treating angina. Beta blockers can also lower the blood pressure.

Answer 3

beta blockers are a class of drugs used to treat high blood pressure and other heart/circulatory conditions. They block the effects of adrenaline on the body's beta receptors, and make the heart work less hard to pump blood.

Answer 4

It is an anti-hypertensive medication. It slows down your heart rate, not putting as much pressure on your heart.
Although, it is commonly used for High Blood Pressure, it is also prescribed for Anxiety/Panic, and Tachycardia (rapid heart rate)

Answer 5

Pharmacology
Beta blockers block the action of endogenous catecholamines, epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular, on β-adrenergic receptors, part of the sympathetic nervous system 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, kidney, and adipose tissue. β2-Adrenergic receptors are located mainly in the heart, lung, GI tract, liver, pancreas, and skeletal muscle. The role and location of β3-receptors is less well-defined.

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β-Receptor antagonism
Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β2 receptors induces smooth muscle relaxation (resulting in vasodilation and bronchodilation amongst other actions), induces tremor in skeletal muscle, increases glycogenolysis in the liver and skeletal muscle.

Beta blockers inhibit these normal epinephrine-mediated sympathetic 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, opening of bronchi, reduce tremor, and breakdown of glycogen.

It is therefore somewhat unexpected that non-selective beta blockers have an antihypertensive effect, since they appear to cause vasoconstriction. The antihypertensive mechanism appears to involve: reduction in cardiac output (due to negative chronotropic and inotropic effects), reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity.

Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand.

The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade – resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.

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Intrinsic sympathomimetic activity
Some beta blockers (e.g. oxprenolol and pindolol) 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 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 (Rossi, 2006).

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α1-Receptor antagonism
Some beta blockers (e.g. labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.

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Other effects
Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbance caused by some agents (Stoschitzky et al., 1999).