Alpha-1 agonist and venous tone

[OphthLover]

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I read from UWorld that alpha1 agonist such as phenylephrine (a1>a2) decreases CO because of the combined effects of increased sympathetic tone (vasoconstriction) from alpha2 and vascoconstriction from alpha1. The answer also stated that the agonist would also decrease preload or venous return.

1. But wouldn't sympathetic activation from alpha1 receptor elevate HR, and thus would compensate for the increased TPR, and maintain constant CO?
2. I think I read from other sources that alpha1 agonist activity includes increasing venous tone (venoconstriction). Shouldn't the drug then increas the venous return?
3. What's the alpha2's effect on venous tone?

I'd appreciate any help!

 

[Psai]

Phenylephrine is a selective alpha1 agonist. Im not sure if it has enough alpha 2 to be clinically relevant. You get a reflex bradycardia due to increased prrssure on aortic arch baroreceptors and carotid sinus. Decreases hr. Beta 1 agonists would increase hr, not alpha1.

Alpha1 should increase venous tone and return

http://cvpharmacology.com/vasodilator/alpha this should help with question 3

 

[Entadus]

But wouldn't sympathetic activation from alpha1 receptor elevate HR

No. The activation of alpha1 receptors by an alpha1 agonist (DRUG) is not sympathetic activation (since the agonist is not coming from sympathetic nerves). Besides, the heart (rate, contractility, etc) is sensitive to sympathomimetics through the activation of BETA-1 receptors, not alpha. The primary effect of alpha-1 stimulation would be on the peripheral vessels (arteries>veins) causing constriction and therefore increased peripheral resistance. Afterload increases and preload decreases

 

[OphthLover]

Afterload increases and preload decreases

Thank you both for your answers. Since a1 increases venous tone as well, wouldn't it increase preload?

 

[Entadus]

Thank you both for your answers. Since a1 increases venous tone as well, wouldn't it increase preload?

No. Blood flows from the great veins into the right atrium due to a (driving) pressure gradient (pressure difference between SVC/IVC and the RA). By increasing vascular resistance (most of which would be in the arterioles, some in the venules and veins), blood will be lower pressure by the time it reaches the veins and will not have a high driving pressure to enter the heart. Preload (and venous return) would decrease

 

[SpacemanSpifff]

No. Blood flows from the great veins into the right atrium due to a (driving) pressure gradient (pressure difference between SVC/IVC and the RA). By increasing vascular resistance (most of which would be in the arterioles, some in the venules and veins), blood will be lower pressure by the time it reaches the veins and will not have a high driving pressure to enter the heart. Preload (and venous return) would decrease

Mmmmm, maybe. Check this out: http://jap.physiology.org/content/113/2/281.long.