Vasodilatation by acetylcholine is endothelium‐dependent: a study by sonomicrometry in canine femoral artery in vivo.

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Abstract
The external diameter of the femoral artery was measured by sonomicrometry in the anesthetized dog. Intra-arterial acetylcholine lowered arterial pressure and thereby passively lowered diameter. When blood flow and distal resistance were controlled by roller pump and Starling resistor, respectively, acetylcholine (0.1-10 .mu.M) and substance P (0.1-1 nM) both caused up to a 10% increase in diameter. Removal of endothelium by mechanically rubbing the artery lumen abolished to the dilator response to acetylcholine and substance P but did not affect the response to nitroprusside. Constrictor responses to noradrenaline [norepinephrine] were unaltered by endothelium removal. Topical application of acetylcholine and substance P onto the adventitial surface of the artery also caused an increase in diameter but both agents were 50-100 times less potent by this route compared with intra-arterial infusion. These dilator responses were abolished by endothelium removal. In these circumstances acetylcholine caused constriction. Acetylcholine and substance P evidently require an intact endothelium to elicit vasodilatation in vivo, at least for the large femoral artery. The topical application experiment suggests that local neural release of vasoactive substances such as acetylcholine and substance P depend on an intact endothelium to cause vasodilatation.