QUESTIONS

1. Where might one find Beta-one receptors & what effect will they cause when stimulated?  How about Beta-two receptors?
    
2. What is the difference between alpha receptors & beta receptors?
    
3. In early CHF, the beta one receptors are stimulated & the heart is able to recompensate thanks to that stimulation (hopefully).  Why can't the symp N.S. just keep the heart compensated long term?
    
4. Which beta receptors are blocked by "beta blockers?"
    
5. How is propranolol thought to assist in treating arrhythmias (& list a few arrhythmias that it might be good for).
    
6. List as many circumstances as you can think of where it might be bad to give propranolol.  (I thought of 6)
    
7. What happens to Beta one receptors with chronic use of beta blockers?
    
8. Why are beta blockers helpful in treating hypertension?
    
9. What might be some uses for beta blockers that don't involve heart disease?
   
   
   
   
    

ANSWERS

1. Beta-one receptors are found in the heart. When stimulated, they increase heart reate, AV conduction, & automaticity.
   
   Beta-two receptors serve to dilate bronchial & vascular smooth muscle.
   
   
   
   
    
2. The difference between alpha & beta receptors is pharmacological.  In the sympathetic nervous system, the neurotransmitter between the fiber & the effector organ is norepinephrine regardless of whether the receptor is alpha or beta.  However, alpha receptors tend to respond better to norepi than to epi or isoproteranol.  Alpha receptors are blocked by phenoxybenzamine.  Betas respond better to epi or isoproteranol than to norepi.  Betas are blocker by dichloroisoproteranol.
   
   (I am a little confused about where one finds alpha receptor & what they do.  Alpha ones will constrict vascular smooth muscle. What about alpha twos?)
   
   
   
   
    
3. Well aside from the extra volume our friend aldosterone has provided for the compromised heart to pump & the extra afterload courtesy of angiotensin 2, the B-1 receptors "down regulate" w/chronic symp. n.s. stimulation. This means the B-1 receptors actually have conformational changes & disappear leaving the heart less responsive to the symp. N.S.
   
        *  Hyperthyroidism will "up-regulate" the receptors
   
        *  Hypothyroidism will "down-regulate" the receptors
   
        *  The aging process will "down-regulate" the receptors.
   
   
   
   
    
4. Trick Question!  There are many beta blockers. Some block exclusively beta one receptors. Some (like propranolol) will block both beta one & beta two receptors.  Some do some alpha blocking on the side & one (pindolol) has "intrinsic sympathomimetic activity," meaning that it's overall effect is stimulating to the symp. N.S.
   
   
   
   
    
5. Propranolol slows the discharge of the SA node & of ectopic pacemaker tissue & slows conduction throught the AV node.  This is a good thing when you have an arrhthmia of increased automaticity such as atrial fib, supraventricular tachyarrhytmia, or digoxin toxicity arrhthmias.
   
   (Paul, our text book notes they are used also in ventricular arrythmias. When would you pick a beta blocker over say lidocaine or procan for a ventricular arrhythmia?)
   
   
   
   
    
6. a) Sick sinus syndrome:  This would be a very bad time to slow discharge at the SA node.
   
   b)  Asthma: propranolol is a Beta 1 & 2 blocker.  This could lead to unopposed alpha one tone & bronchoconstriction can result. A pure Beta one blocker wouldn't do this.
   
   c)  CHF:  Beta blockers are bad negative inotropes & this patient may be depending on its symp. N.S. to stay alive.  (But just in case there's alos an arrythmia you want to convert & you want to use the beta blocker but you are concerned about the CHF, you can try esmolol which has a very short half life & is given as a drip & if it isn't working out the way you planned, you can easily d/c it.)
   
   d)  Concurrent use of Negative inotropic drugs: like a calcium channel blocker or lidocaine type anti-arrhthmic.These drugs with a beta blocker will pretty much take out contractility.
   
   e)  Diabetes Mellitus:  Propranolol has caused some nasty hypoglycemia.  (Paul, do we know the mechanism responsible?)
   
   f)  Saddle thrombus:  Tempted to put that HCM cat on propranolol? You might want to wait until the legs have reperfused since propranolol can reduce tissue perfusion.  (Paul, is this because of reduced cardiac output or vasoconstriction or what?)
   
   
   
   
    
7. Because of negative feedback, beta one receptors will up-regulate with chronic beta blocker use.  (Paul, what is the clinical signif, of this?  I've read that some are attributing good results due to symp. NS support now that the receptors have been up regulated yet we've been trying to block them.  Please explain this paradox.)
   
   
   
   
    
8. We don't know :)
   
   We hav theories.  It could be that reducing contractility & HR lead to reduced blood pressure.  It could be reduced renin secretion via the non-selective beta blockers (Paul, did I read this correctly?  I though renin secretion was independent of the symp. NS.  Plus, I'd have thought we'd get vasoconstriction by blocking Beta two receptors.  How is it possible that we can treat hypertension w/a beta blocker ? And what other theories should I present?)
   
   
   
   
    
9. Beta blockers can be used for the treatment of caffeine toxicity, cocaine toxicity & for pheochromocytoma (but you must also use an alpha blocker to avoid hypertension.)
   
   Paul, is there anything else that needs to be added? I've found the beta blocker subject to be a bit confusing due to all the different types of beta blockers (which principles are true for all beta blockers & which are true for just propranolol?)