The binding affinity to and receptor of epinephrine at different dose

[hpw]

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I read it on my pharmacology text book:
at low dose,epinephrine has greater effect on β receptor than α receptor
at high dose,epinephrine has greater effect on α receptor than β receptor
and I know
the affinity for α receptor :epinerphrine>norepinephrine>isoproterenol
for β receptor :isoproterenol>epinerphrine>norepinephrine
but how can I explain the different affinity of epinephrine to α and β receptor at different dose?

 

[ucladoc2b]

I read it on my pharmacology text book:
at low dose,epinephrine has greater effect on β receptor than α receptor
at high dose,epinephrine has greater effect on α receptor than β receptor
and I know
the affinity for α receptor :epinerphrine>norepinephrine>isoproterenol
for β receptor :isoproterenol>epinerphrine>norepinephrine
but how can I explain the different affinity of epinephrine to α and β receptor at different dose?

Keep in mind there are two predominant beta receptors (well, actually 3 now that I think about it). EPI has very high affinity for the B2 receptor vs. Norepi. The B2 receptors are more predominant in skeletal muscle, which is why you see a decline in BP with low dose EPI. At a physiological (low) dose, the beta effects will tend to predominate. As the dose is increased, EPI binds to more alpha receptors, at which point, alpha receptor BP effects will tend to dominate.

 

[hpw]

thank you for answering and I have another question:
why does EPI cause increasing of systolic blood pressure and "decreasing" of diastolic pressure at low dose?

 

[Scilencer]

Hits b1...increase heart contraction strength
Hits b2...dilates smooth muscle (vessels)

So with a low dose you got increased heart contractility (elevated systolic) but more dilated vessels (decreased diastolic) since the CV system has higher "capacitance".

 

[ucladoc2b]

thank you for answering and I have another question:
why does EPI cause increasing of systolic blood pressure and "decreasing" of diastolic pressure at low dose?

I answered the question for you above. Keep in mind, EPI and NE work on the autonomic nervous system (fight or flight or rest and digest). Where would you need more blood during times of stress, your stomach or your skeletal muscles? How do you get more blood to these places? What is the receptor on these targeted tissues? And what is responsible for systolic blood pressure?

 

[hpw]

thank you for answering