Acetylcholine induces contractile and relaxant effects in canine nasal venous systems

¹ Dept of Physiology, Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.

^* To whom correspondence should be addressed. E-mail: makylung{at}hkucc.hku.hk.

	Abstract

Acetylcholine induces nasal congestion at low dose but decongestion at high dose. This study investigated the vascular mechanisms underlying this biphasic nasal airway response in the dog.

Collecting and outflow veins from anterior and posterior nasal venous systems and the septal mucosa (containing sinusoidal venous plexuses) were isolated. In vitro isometric tension of the vascular segments was monitored to reflect vascular reactivity. Immunohistochemical localization of NADPH-diaphorase and eNOS was performed.

Acetylcholine did not affect the venous plexuses but concentration-dependently contracted anterior collecting vein and outflow veins of both systems; the responses were unaffected by L-NAME. Acetylcholine relaxed posterior collecting veins at low concentrations but contracted them at higher concentrations; L-NAME enhanced the contractions but inhibited the relaxations with the inhibition reversed by L-arginine. NADPH-diaphorase and eNOS were located predominantly in the posterior collecting veins.

That acetylcholine at low concentrations relaxes posterior collecting veins but contracts other collecting and outflow veins implies that the agonist in vivo may induce nasal congestion by increasing posterior blood volume. At higher concentrations, acetylcholine contracts posterior collecting veins as well, implying diminished blood volume in both venous systems, subsequently nasal decongestion. The induced-contraction in posterior collecting veins is NO-independent while the induced relaxation is NO-dependent.