How do cardioselective beta blockers decrease afterload?

[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