Jul 6, 2016
10
0
I'm a bit confused with epinephrines mechanism of action in low doses.

It acts on alpha 1 receptors in the venous system, increasing venous return. I'm not entirely sure this is the right mechanism (correct me if I'm wrong) but by increasing venous return, it increases preload, which increases SV and thus increasing the amount of blood in the arterial system, increasing diastolic pressure. However in low doses, it acts more on b2 receptors, dilating skeletal arterioles and this outweighs the a1 venoconstriction, to overall decrease diastolic BP. (is this correct?)

Meanwhile it also acts on a1 receptors in systemic arterioles, increasing systolic pressure.

I might have this completely backwards. But I'm having difficulty tying in all the receptor effects to their corresponding changes in diastolic/systolic BPs.
 
OP
M
Jul 6, 2016
10
0
There seems to be a discrepancy in what alpha-1 constriction does to systolic/diastolic BP in the arteriole/venule circulation.

Sketchy pharm says that alpha-1 arteriolar constriction increases systolic blood pressure, and alpha-1 venous constriction increases diastolic blood pressure.

I watched Najeeb's lectures on the autonomic system. He says that alpha-1 arteriolar constriction increases the TPR, and prevents arteriolar blood from passing through the arterioles there by increasing diastolic blood pressure. He then explain that alpha-1 venous constriction causes an increase in venous return, a subsequent increase in preload and increase SV which causes an increase in systolic blood pressure.

Najeeb's explanation makes more sense to me. Can anyone confirm that this is correct?
 
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