Effects on nasal nitric oxide production of 2 mechanisms of vasoconstriction

Vasoconstrictor drugs reduce nitric oxide (NO) production in vitro by inhibiting the enzyme involved in the regulation of inducible and constitutive NO synthases (iNOS and cNOS). Intranasal vasoconstrictors also decrease nasal NO concentration in vivo. It is as yet unclear if this last finding is due to the effects of the drug on the enzyme or on the vessels. Physical exercise also induces nasal vasoconstriction and reduces nasal resistance.

The aim of this study was to clarify the mechanisms involved in xylometazoline-induced reduction of nasal NO concentration.

We compared 2 randomized groups of patients with moderate--severe persistent allergic rhinitis. The first group (n = 24) underwent a physiological nasal vasoconstrictor stimulus (exercise) whereas the second group (n = 29) was treated with a nasal vasoconstrictor drug (topical xylometazoline). Nasal volume and NO were determined at baseline and 15 to 20 minutes after the end of each stimulus using acoustic rhinometry and chemiluminescence, respectively.

Baseline values of nasal volume and NO did not differ between the 2 groups. Nasal volume increased by 57% (P = .0001) after exercise and 71% (P = .0001) after xylometazoline. Nasal NO decreased (25%, P = .001) after xylometazoline, but not after exercise.

Physical exercise and topical xylometazoline cause vasoconstriction and similar effects on nasal volume. In contrast nasal NO decreased with xylometazoline but not after exercise. These findings suggest that vasoconstrictor drugs reduce nasal NO by mechanisms other than vasoconstriction.