Why is there a systolic BP increase in the control case with low doses of Epi?
At low dose EPI is acting mainly at beta-receptors with a little alpha-receptor activity. At low doses EPI acts on the beta1-receptors to increase CO and hence BP. Some vasoconstriction (alpha1-action) to increase TPR and hence BP. These two actions are the cause of the increase in systolic BP. Finally vasodilatation via an action on beta2-receptors to decrease TPR and hence decrease BP. The overall effect on peripheral resistance at low dose is a fall in TPR (beta2-effect is greater than alpha1-effect).
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