Blood vessels throughout the body mostly aren't supplied by any parasympathetic fibres. But the effects of ACh through M3-ACh receptors would infact release NO (which acts on VSM and causes vasodilation), which is demonstrated after ACh intravenous administration.
My question is how is it physiologically mediated? (i.e. the ACh mediated vasodilation)
*VSM= vascular smooth muscle *NO= Nitric Oxide *Ach= Acetylcholine *M3 (Muscarinic type 3) Acetylcholine receptor