Step I Atenolol
Started by busy08
Atenolol is beta-1 selective, so it should reduce cardiac contractility without dilating arterioles. Therefore, decreased systolic BP.
Atenolol, out of any of the beta-blockers, is also the 1st-line Tx for social phobia (e.g. public speaking).
Atenolol, out of any of the beta-blockers, is also the 1st-line Tx for social phobia (e.g. public speaking).
Wasn't propranolol used for that?
Yes. Any beta blocker will do, but usually propranolol
Atenolol is abused to reduce shaking, though, in performance sports (like hand gun shooting).
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Simply to say ALL beta blockers reduce blood pressure.
Question for you: how would atenolol NOT lower BP in a normal person, but still be able to lower it in pathological states?
My hypothesis: some sort of BP-sensitive moiety on the molecule that results in activation of the drug only when it senses systolic P > 140. This conveniently mirrors different set points for hypertension; in diabetics, the drug activates at 130 mm Hg.
My hypothesis: some sort of BP-sensitive moiety on the molecule that results in activation of the drug only when it senses systolic P > 140. This conveniently mirrors different set points for hypertension; in diabetics, the drug activates at 130 mm Hg.
I had encountered atenolol as the answer to a practice question some time ago regarding social phobia. It was also specifically mentioned by my PBL tutor last year.
I can't recall offhand. However, although this is not in support of my point, I believe it just listed atenolol and not propranolol. So, no, the question didn't differentiate between those two as much as it did just cite atenolol.
I feel like this may have been a Kaplan Qbook question, but I'm not 1000% sure.
It just randomly occurred to me that atenolol would unquestionably be a much better choice over propranolol for social phobia.
If you block both beta-1 and -2 receptors with propranolol, then when the patient gets an SNS response because he or she is nervous, he or she would then get a spike in BP because of unopposed alpha-1 (same reason you don't give beta-blockers to PCO patients).
With atenolol, the increased SNS response in the social situation wouldn't produce the same increase in BP because beta-2 is still activated alongside alpha-1, thereby attenuating any net vasoconstrictive effects.
Therefore atenolol must be the better choice over propranolol.
If you block both beta-1 and -2 receptors with propranolol, then when the patient gets an SNS response because he or she is nervous, he or she would then get a spike in BP because of unopposed alpha-1 (same reason you don't give beta-blockers to PCO patients).
With atenolol, the increased SNS response in the social situation wouldn't produce the same increase in BP because beta-2 is still activated alongside alpha-1, thereby attenuating any net vasoconstrictive effects.
Therefore atenolol must be the better choice over propranolol.
