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Parasympatholytic vs. sympathomimetic drug


Function

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A question that was asked on a previous edition of the exam concerning the cardiovascular system, was:

 

Nose decongestion, hypertension and mydriasis may be evoked by a

  • Parasympatholytic
  • Sympathomimetic
  • Parasympathomimetic
  • Sympatholytic

Of course, the last 2 are false.

Now, there is a big discussion on which of the 2 remaining would be the correct answer.

 

I plead for the sympathomimetic, whereas others prefer the parasympatholytic.

 

Arguments for parasympatholytic:

  • Removal of the sympathetic inhibition by the parasympathetic nervous system
  • Inhibition of the parasympathetic effects by the vagus nerves on SA and AV nodes, increasing heart rate

Arguments for sympathomimetic:

  • Activation of myocard, smooth muscle cells in coronary arteries and also the SA and AV nodes
  • Peripheral vasoconstriction (alpha-1) which, as far as I'm aware of, can not be evoked by blocking parasympathetic NS?
  • Activation of the renine-angiotensin-aldosteron system by activation of renal beta-1 receptors

I think that, mainly because of the last 2 reasons, a sympathomimetic would be more useful to evoke hypertension.

 

Thoughts?

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Yep I think you are right. Vascular smooth muscles are controlled by SNS but not PSNS. That's why nasal decongestants are mostly sympathomimetics like ephidrine and pseudoephidrine. Also you see epinephrine combined with local anaesthesia to prolong the anaesthetic effects, but not parasympatholytics.

 

To me this may be the major differentiating factor, since muscarinic antagonists can give mydriasis. PSNS has more of an effect on HR, but not necessary BP.

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Note that the vascular smooth muscles in nasal mucosa, spongious tissue and salivatory glands (especially parotis gland) are controlled by both SNS and PSNS (they form exceptions), which is why a PSNS-antagonist does indeed relieve nasal congestion (although I don't know why one doesn't give a PSNS-antagonist such as atropine, perhaps because of the unwanted side effects on the heart rate?)

 

Indeed, I think that RR is the differentiating factor here; both PSNS-block (via ACh on muscarinic receptors via Edinger Westphal nucleus and oculomotor nerve) and SNS (via the superior cervical ganglion) may induce mydriasis, seen in oculomotor palsy and Horner's syndrome

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Very well ... Anyway, if the question should appear on the exam, and the answer would've been a parasympathicolytic, then there is enough evidence arguing that a sympathicomimetic would be better (even in the Commented Drugs Repertory 2014 (and perhaps also 2015, don't know; I'll receive the 2016 version next term), the book in which about every drug that can be used as therapy is listed, a book every Belgian doctor has in his lab coat or in his desk, only sympathicomimetics are listed under "nasal vasoconstrictors") and as per result, enough evidence to have the question removed

Edited by Function
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Agree with your post Function.

In some cases they essentially do very similar things. For example,
- Atropine is a muscarinic (parasympathetic) ANTAGONIST - i.e. a parasympatholytic
- Adrenaline/Epinephrine is an agonist at all adrenergic receptors i.e. a sympathomimetic

EITHER can be used in the treatment of bradycardia (slow heart) depending on the circumstances. The parasympatholytic will reduce the parasympathetic effect slowing down the heart, and the adrenaline will increase the sympathetic action speeding up the heart.

A lot of the time however, it will probably depend on the specificity of the drug as to which one is used. I.e. which receptors it works on in order to bring about a specific effect.

There are cases where the drugs are not interchangable and this is because of differences in sympathetic/parasympathetic supply. I can't think of any examples at this minute.

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