sympathetic response question

[str8cashhomie]

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Just to clarify, with the sympathetic response the heart rate increases, pupils dilate, which makes sense because norepi and epi are vasodilators. But where does the increased blood pressure come from? I know the heart rate increases, but increased blood pressure would mean vasoconstriction of blood vessels? why vasoconstrict

 

[The_Sunny_Doc]

Just to clarify, with the sympathetic response the heart rate increases, pupils dilate, which makes sense because norepi and epi are vasodilators. But where does the increased blood pressure come from? I know the heart rate increases, but increased blood pressure would mean vasoconstriction of blood vessels? why vasoconstrict

Vasoconstriction occurs in your internal organs (think of how you can't digest food well when you're running from a tiger... or cramming all night for an exam lol) and vasodilation for your skeletal muscles, which need more O2 as you're trying to flee. Your bp drops with that vasodilation in the muscles, so your body has to constrict the vessels SOMEWHERE (=not in the organs being used to run away or fend off an attack!) to compensate in order to keep bp stable.

 

[sakabato93]

Just to clarify, with the sympathetic response the heart rate increases, pupils dilate, which makes sense because norepi and epi are vasodilators. But where does the increased blood pressure come from? I know the heart rate increases, but increased blood pressure would mean vasoconstriction of blood vessels? why vasoconstrict

You're absolutely right! Blood vessels are constricted, but in the visceral organs (i.e. gut organs) and skin, while the skeletal muscle blood vessels are dilated. This occurs because it induces the shunting of oxygenated blood toward the skeletal muscles which helps facilitate the flight-or-flight response by efficiently facilitating abundant ATP in important muscles.

Now, vasoconstriction is simply caused by the contraction of smooth muscle cells on the inner lining of the arterioles, Poiseuille's Law indicates the vessel pressure is inversely proportional to the radius of the vessel to the forth power, indicating that a very tiny change in smooth muscle conformation is responsible for BIG changes in pressure (Poiseuille's Law:http://hyperphysics.phy-astr.gsu.edu/hbase/ppois.html ; its not necessary to memorize, but its good to look at the math to better understand the concept). Smooth muscle contraction and relaxation is a very efficient way for the body to control blood pressure in the short term.

The mechanism that induces vasoconstriction is a tad more complicated though. As you've mentioned, the sympathetic nervous system uses epinephrine and norepinephrine as their post-ganglionic neurotransmitters to induce desired effects on target organs. Long story short, there is a group of receptors called beta-adrenergic receptor (any adrenergic receptor is one that binds to epinephrine/norepinephrine, aka, adrenaline/noradrenaline). Binding of beta-adrenergic receptors (at a variety of sites including vessels, heart, and kidneys) with the respective neurotransmitter induces a flurry of cellular responses, one of which is vascular smooth muscle contraction in arterioles. Binding of beta-adrenergic receptors in the kidneys induces the release of Renin, and enzyme responsible for the proper activation of angotensin II, which further increases blood pressure through inducing the secretion of aldosterone from the adrenal cortex, among other effects.

I think that summarizes it fairly well. Let me know if you have any questions!👍

 

[image187]

You're absolutely right! Blood vessels are constricted, but in the visceral organs (i.e. gut organs) and skin, while the skeletal muscle blood vessels are dilated. This occurs because it induces the shunting of oxygenated blood toward the skeletal muscles which helps facilitate the flight-or-flight response by efficiently facilitating abundant ATP in important muscles.

Now, vasoconstriction is simply caused by the contraction of smooth muscle cells on the inner lining of the arterioles, Poiseuille's Law indicates the vessel pressure is inversely proportional to the radius of the vessel to the forth power, indicating that a very tiny change in smooth muscle conformation is responsible for BIG changes in pressure (Poiseuille's Law:http://hyperphysics.phy-astr.gsu.edu/hbase/ppois.html ; its not necessary to memorize, but its good to look at the math to better understand the concept). Smooth muscle contraction and relaxation is a very efficient way for the body to control blood pressure in the short term.

The mechanism that induces vasoconstriction is a tad more complicated though. As you've mentioned, the sympathetic nervous system uses epinephrine and norepinephrine as their post-ganglionic neurotransmitters to induce desired effects on target organs. Long story short, there is a group of receptors called beta-adrenergic receptor (any adrenergic receptor is one that binds to epinephrine/norepinephrine, aka, adrenaline/noradrenaline). Binding of beta-adrenergic receptors (at a variety of sites including vessels, heart, and kidneys) with the respective neurotransmitter induces a flurry of cellular responses, one of which is vascular smooth muscle contraction in arterioles. Binding of beta-adrenergic receptors in the kidneys induces the release of Renin, and enzyme responsible for the proper activation of angotensin II, which further increases blood pressure through inducing the secretion of aldosterone from the adrenal cortex, among other effects.

I think that summarizes it fairly well. Let me know if you have any questions!👍

This is good, except for the receptor part which you might want to review. The important adrenergic receptors are...

B1 - cardiac (inc rate, contractility of cardiac muscle), kidney (renin release), fat cells (lipolysis)

B2 - bronchioles (smooth muscle relaxation, dilation), blood vessels (dilates: skeletal muscle, etc...), liver (stimulates glycogenolysis), bladder (inhibits contraction)

a1 - blood vessels (vasoconstriction), Gi (decrease motility), eye (dilator muscle contraction)

a2 - basically supresses adrenergic neurotransmission

 

[sakabato93]

This is good, except for the receptor part which you might want to review. The important adrenergic receptors are...

B1 - cardiac (inc rate, contractility of cardiac muscle), kidney (renin release), fat cells (lipolysis)

B2 - bronchioles (smooth muscle relaxation, dilation), blood vessels (dilates: skeletal muscle, etc...), liver (stimulates glycogenolysis), bladder (inhibits contraction)

a1 - blood vessels (vasoconstriction), Gi (decrease motility), eye (dilator muscle contraction)

a2 - basically supresses adrenergic neurotransmission

I honestly think that this specific stuff is beyond the scope of the MCAT. I didn't cover it in too much detail in my upper level physiology course, and my professor focuses on blood pressure research, so we were all taught kidneys/bp inside and out for class.

 

[image187]

I honestly think that this specific stuff is beyond the scope of the MCAT. I didn't cover it in too much detail in my upper level physiology course, and my professor focuses on blood pressure research, so we were all taught kidneys/bp inside and out for class.

yeah, it probably is way too specific for the MCAT. At a bare minimum in terms of adrenergic receptors though one may want to remember that in general:

a1 - vasoconstriction
B2 - vasodilation

 

[sakabato93]

yeah, it probably is way too specific for the MCAT. At a bare minimum in terms of adrenergic receptors though one may want to remember that in general:

a1 - vasoconstriction
B2 - vasodilation

Right, but each receptor is in a different effector organ.

a1 would be in vessels of gut organs and B2 would be in skeletal muscles, correct?

 

[image187]

Right, but each receptor is in a different effector organ.

a1 would be in vessels of gut organs and B2 would be in skeletal muscles, correct?

well in a simplistic sense yeah, but really, the receptors are everywhere but there is an overall net effect of which ones dominate during a given response based on local receptor concentration, and which molecules activate them. For instance, there are both alpha and beta adrenergic receptors on the smooth muscle of the bronchioles, however the B2 (dilation) obviously dominates. Hence, epinephrine having a net dilatory effect on the bronchioles.

Also, epinephrine has action at all of these receptors (In addition to other adrenergic substances) but norepinephrine essentially only has action at a1, a2, and B1 receptors, and negligible B2 activity. This is why norepinephrine will not work as a bronchodilator. it has effects on blood pressure during sympathetic flight or fight, but will have essentially no effect on skeletal muscle vessel dilation, and will not stimulate glucagon secretion

 

[KDVMSPH]

Great Question!

I love this topic! How I remember the sympathetic system is by thinking realistically! When the sympathetic kicks in 'fight or flight', simply think of what your body would natural do. If you are running for your life, your blood pressure will more than likely increase = vasoconstriction. Your pupils will dilate, so you can see better. Digestion will decrease, because your body really doesn't have time to be digesting food and allotting energy to the stomach!

These questions are frequent on the MCAT so make sure you know the difference between fight and flight and rest and digest! Good luck!! 🙂