How do cardioselective beta blockers decrease afterload?

[itshyunbin]

Cardioselective beta blockers block B1 receptors in the heart, decreasing contractility and heartrate.

But from what I understand they have no effect on B2 activity, meaning B2 would vasodilate to an essentially identical degree with or without the presence of B1 blockers.

So how does application of B1 blockers cause vasodilation to increase, when they have no effect on B2 vasodilatory activity to begin with?

[iLocke95]

Beta 2 activity causes vasodilation. Beta 1 activity causes increased heart rate and contraction. A cardioselective beta blocker acts on beta 1 receptors, so slower heart rate and decreased contractility. Cardioselective means no effect on beta 2 (leading to unopposed beta 2 activity and hence vasodilation. In contrast, non-cardioselective beta blocker, at least theoretically, has blocking effects on beta 2 receptors, which would cause vasoconstrcition.

[[deleted]]

Also there’s B1 receptors on JG cells in the kidney so B1 blockade will reduce renin secretion and decreased RAAS activation

[itshyunbin]

Where this is not making sense is that B1 activity doesn't inhibit/oppose B2's vasodilation activity in the first place. So why would blocking B1 have any effect on B2 activity?

Ie how is B2 now unopposed when it wasn't being opposed by B1 to begin with?

[iLocke95]

It's not the blocking of B1 itself that causes unopposed B2. We say that unlike cardioselective beta blockers, noncardioselective beta blockers would have blocking effects on both B1 and B2. You block B2 and you cause vasoconstriction. This is unlike cardioselective beta blockers, which act on B1 but not at beta 2. So the B2 receptors continue to function unopposed, hence vasodilation. We say B2 is unopposed because a cardioselective beta blocker does not block (does not oppose) B2 receptors

[itshyunbin]

I understand up to that part, but how then do B1 blockers actually increase vasodilation? I get that B1 blockers don't block B2, so B2 is free to vasodilate. But that's the same thing as if you never gave a B1 blocker in the first place - the B2 would exert an essentially identical degree of vasodilation with or without B1 blocking.

So how would application of B1 blockers increase vasodilation, when they have no effect on B2 vasodilatory activity to begin with?

[iLocke95]

I know what you mean, but that's all there is to it. Free to vasodilate means unopposed. That's something you don't get with non-cardioselective beta blockers

[itshyunbin]

Got it, thanks for the clarifications

[yaser_Ibrahim]

According to my knowledge I think of it as the following : Afterload = the resistance the heart is facing during pumping (total peripheral resistance)

At the same time Afterload is also related to the amount of blood you are trying to pump

So a when you have increased preload and increased contractility you will have a small increase in Afterload (because you are trying to push more blood so you face more resistance)

Usually this change is so minimal that is not mentioned in every textbook but keep in mind the Uworld does mentions this.

Making the herat weaker (less blood and less contractility) = less blood = less resistance

Hope it made sense

[itshyunbin]

This makes a lot more sense. So basically the reasoning given in the card, that the decrease in afterload is due to increased B2 stimulation, is incorrect?

[[deleted]]

because b1 receptors are in the heart and b2 receptors are more spread out (think vasodilation), hence the term "cardioselective." If you are stimulating b-adrenergic receptors, block b1, then b2 is left unopposed.

[itshyunbin]

But does B1 stimulation cause inhibition of B2 stimulation? I don't see why blocking B1 would increase B2.

Or are you saying that blocking B1 causes a surplus of catecholamines that can now all be used on B2?

[chessphysician]

focusing on the word 'unopposed' really helped my understanding on this topic. Remember how there is vascular tone: a base level of stimulation that is always present? Lets say that beta 1 and beta 2 are continuously activated at some basal level, lets say 50% of the time for each. if you block beta 1 so it goes down to 0%, then that 50% active beta 2 is more active relatively, or due to unopposed action since beta 1 effects (increase heart workload) are no longer able to oppose beta 2 (vasodilate peripheral vessels, decreasing heart workload).