Information on Beta Blockers

Subj: Beta Blockers... some info
Date: 97-03-14 20:45:56 EST
From: Shaun
To:

Hey Claudia...

I did a quick search on the old Internet and found just a ton of info on beta blockers, some with pretty pictures of bond sites that become 3D if you cross your eyes. B) Lemme see if I can explain them without giving you a migrane... for adrenaline molocules to take effect (making you jumpy, excited, etc..) they have to meet up with bonding sites inside the body. These sites are specifically shaped to accept the 3D structure of an adrenaline molocule and nothing else. It's kind of like a complex lock and key mechanism. When the adrenaline locks into the beta receptor site it causes the body to absorb the molocule and use its energy to pep you up (or in your case, tire you out!). What beta blockers do is mimic the shape of the arenaline, so they will fit into the beta receptor... but once they are there they latch on rather than releasing anything into the body. By doing this they in effect "block" the site, preventing the real adrenaline molocules from entering. You can always tell a beta blocker by its name. If it's generic (not corporate) name ends in -olol you can bet that it's keeping SOMETHING from doing its job. There's your crash course in beta blockers! You didn't even have to learn about folding or chirality or handedness... you should feel lucky! :D

I'm sending along a website about beta blockers that you don't actually need 4 PhDs to understand... scientist can be really interesting people, but you wouldn't know it from the articles they publish! (By the way, if you want to know more just find a web search site and type "Atenolol beta blockers" or something to that effect... you'll find TONS of stuff!)

Talk to you some more later on... I just wanted to send you this while it was fresh in my head.

--Shaun
 

Beta Blockers

Cardioselective (Selective beta 1 blocker)
Generic Name (Other Names)

Acebutolol (Sectral)
Atenolol (Tenormin)
Betaxolol (Kerlone)
Bisoprolol (Zebeta)
Metoprolol (Lopressor)

Non Selective (Blocks beta 1 and beta 2 equally)
Generic Name (Other Names)

Carteolol (Cartrol)
Nadolol (Corgard)
Penbutolol (Levatol)
Pindolol (Visken)
Propranolol (Inderal)
Timolol (Blockadren)
Labetalol (Normodyne, Trandate)

Beta Blockers + thiazide diuretic Combinations

Lopressor HCT
ZIAC
Tenoretic
Corzide
Timolide
Inderal LA 40/25
Inderide
Normozide

Beta blockers are one of two antihypertensives classes recommended by an expert panel to for antihypertensive therapy. The other class is thiazide diuretics.

Beta blockers block mainly adrenaline's (epinephrine) effects on the body's beta receptors. There are two primary beta receptors appropriately named beta 1 and beta 2 (There is a beta 3 receptor found in adipose tissue which probably plays a role in obesity.) Some beta blockers are 'selective' meaning that they block beta 1 receptors more than they block beta 2 receptors.

To understand their uses and their effects (including their adverse effects) you have to understand what effects stimulating a beta 1 or a beta 2 receptor will result in.

Beta 1 Receptor

Beta 1 receptors are found primarily in the heart. To understand what effects blocking the beta 1 receptor causes, let us first look at what stimulating these receptors will do. Stimulating beta 1 receptors causes the heart to beat faster (positive chronotropic effect), beat stronger (positive inotropic effect), and causes nerve-muscle conduction velocity to increase (positive dromotropic effect). In addition to the cardiac effects, activating beta 1 receptors also leads to the release of an enzyme in the kidneys called renin, which ultimately leads to vasoconstriction (and thus increases blood pressure as well.)

Therefore, blocking the beta 1 receptor (and all beta blockers block the beta 1 receptor) results in the heart rate slowing down and the heart beating less forcefully. This causes the heart to require less oxygen, less blood is ejected from the heart and blood pressure is lowered. All beta blockers have a "cardioprotective" effect. We do not fully understand how beta blockers have this protective effect on the heart but they do.

Beta blockers are a fundamental treatment in myocardial infarctions (MIs, "Heart Attacks"). They are proven to decrease mortality in patients who have had heart attacks. Beta blockers are only one of two classes of drugs proven to decrease mortality in long-term studies looking at high blood pressure (the other class of drugs are thiazide diuretics.)

The main beta 1 selective drugs used are metoprolol (Lopressor) and atenolol (Tenormin), both are available as generics, and both are proven to benefit patients who have had a myocardial infarction.

Beta 2 Effects

All Drugs which block beta 2 receptors also block beta 1 receptors.

Again, let us first talk about what happens when these receptors are activated and then we will talk about the effects when we block this receptor. Stimulating the beta 2 receptor causes smooth muscle (muscles that control body functions which you do not have control over) to relax. This means that lungs relax (bronchodilation), uterus relaxes, and arterioles (a type of blood vessel) relax. They also cause skeletal muscles (as in biceps, triceps, etc.) to become activated and large.

Blocking these effects then may cause bronchoconstriction or bronchospasms. They may also prevent vascular spasms which may play a role in migraine headaches, and prevent shakiness from "stage fright" and also from low blood sugar (hypoglycemia).

Therefore, drugs which block the beta 2 receptor have adverse effects and uses in addition to the effects mentioned for beta 1 blockade.

The classic non-selective beta blocker is propranolol (Inderal).

Uses of the Beta Blockers

Beta 1 selective or Non-selective

Hypertension
Angina
Supraventricular Tachycardia
Sinus Tachycardia
Ventricular Tachycardia
Premature Ventricular Contractions
Atrial Fibrillation (AFIB) - now recommended as first line therapy.
Myocardial Infarction ("Heart Attack")
Digoxin-induced Arrhythmias
Intraoccular Pressure Reduction
Diastolic Left Ventricular Dysfunction (Diastolic "Heart Failure")
Probably Systolic Left Ventricular Dysfunction if dose is started very low and titrated up VERY slowly.

Additional uses for non-selective beta blockers

Anxiety ("Stage Fright")
Migraine headache prevention
Tremors
Alcohol Withdrawal Syndrome
Esophageal varices
Pheochromocytoma
Thyrotoxicosis

Adverse Effects

Ziac, a selective beta blocker plus a low dose thiazide diuretic, claims to have no more adverse effects than placebo at low doses.

Hypotension (low blood pressure) - all agents which lower blood pressure can make you feel tired, but this effect diminishes usually in a month or two.

Bradycardia (Too slow of a heart rate) Sexual dysfunction (more likely to occur with non-selective agents) Joint Pain and Muscle Cramps have been reported.

A-V Block (risk increases with concurrent digoxin or other heart rate slowing agents) Cardiac Failure (but can be used to treat failure as well) Wolff-Parkinson-White Syndrome (a severe bradycardia) Bronchospasm (primarily with non-selective beta blockers, but can occur with beta 1 selective agents. Blunt signs of hypoglycemia in patients with diabetes mellitus. Increase in triglyceride levels (higher dosages usually) Increase cholesterol levels (higher dosages usually)

The following information was submitted by Claudia Dizenzo, A very special thanks goes out to Claudia for taking the time to put it all together