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    So the sympathetic fibres have bronchodilatory effects whilst the parasympathetic have broncho-constricting effects which makes sense to me.

    But can someone explain how/why sympathetic fibres are vasoconstrictions and inhibit mucus secretions whilst parasympathetic are vasodilators and increase mucus secretions?
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    Hi,

    Sorry for super-late response: just looked at all your threads today and noticed some are still unanswered - hopefully, I can make some concepts simpler for you.

    The adrenergic receptors on the circular smooth muscle of the tunica media of arterioles are alpha-1 receptors, and stimulaion of alpha-1 receptors by noradrenaline leads to activation or agonist activity causing contraction of this smooth muscle (circular) resulting in narrowing of the arteriolar lumen = vasoconstriction.

    Parasympathetic fibres supply the longitudinal muscle of the arterioles (which, if you look at a cross-section of an arteriole) is external to the circular muscle fibres, so their contraction by the action of ACh causes widening of lumen = vasodilatation.

    As regards mucus secretion, most vegetative functions of the body (digestion, micturition, resting heart rate) are controlled/modulated by parasympathetic tone - you must remember that any determination of a physiological autonomic modality is the result of the balance between sympathetic and parasympathetic activity - since the innervation of the mucus glands (in common with that of intestinal ones) is parasympathetic, increase in activity of the parasympathetic causes increased secretion, while increase in sympathetic activity does the opposite.

    A similar situation exists in the buccal cavity - secretion of saliva (at least the aqueous part of it) is mediated by the parasympathetic system via muscarinic receptors; therefore e.g. drugs with an anti-muscarinic side effect e.g. older antihistamines like promethazine or chlorpheniramine AND older anti-psychotics e.g. chlorpromazine, thioridazine produce the side-effect of xerostomia (dry mouth).

    Thanks,
    M.
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    (Original post by macpatelgh)
    Hi,

    Sorry for super-late response: just looked at all your threads today and noticed some are still unanswered - hopefully, I can make some concepts simpler for you.

    The adrenergic receptors on the circular smooth muscle of the tunica media of arterioles are alpha-1 receptors, and stimulaion of alpha-1 receptors by noradrenaline leads to activation or agonist activity causing contraction of this smooth muscle (circular) resulting in narrowing of the arteriolar lumen = vasoconstriction.

    Parasympathetic fibres supply the longitudinal muscle of the arterioles (which, if you look at a cross-section of an arteriole) is external to the circular muscle fibres, so their contraction by the action of ACh causes widening of lumen = vasodilatation.

    As regards mucus secretion, most vegetative functions of the body (digestion, micturition, resting heart rate) are controlled/modulated by parasympathetic tone - you must remember that any determination of a physiological autonomic modality is the result of the balance between sympathetic and parasympathetic activity - since the innervation of the mucus glands (in common with that of intestinal ones) is parasympathetic, increase in activity of the parasympathetic causes increased secretion, while increase in sympathetic activity does the opposite.

    A similar situation exists in the buccal cavity - secretion of saliva (at least the aqueous part of it) is mediated by the parasympathetic system via muscarinic receptors; therefore e.g. drugs with an anti-muscarinic side effect e.g. older antihistamines like promethazine or chlorpheniramine AND older anti-psychotics e.g. chlorpromazine, thioridazine produce the side-effect of xerostomia (dry mouth).

    Thanks,
    M.
    Thank you so much!
    I thought I understood this, but you just made it so much more clearer to understand
 
 
 
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