[Effects of topical alpha 1- and beta 2-adrenoceptor stimulants on nasal nitric oxide level].
The effects of locally administered alpha 1- and beta 2-stimulants (naphazoline and salbutamol) on the nasal nitric oxide (NO) level were investigated. Twenty-four healthy volunteers (except nasal allergy) were subjected to the examination. First, nasal cavity air was sampled continuously from the right nostril for 20 seconds at the rate of 3.5 l/m, and NO-free air was supplied passively to the left nostril. During the sampling time, subjects were made to hold their breath at deep inspiration, which obviated the effect of lower airways by closing their glottises. The sampled air was analyzed using a chemiluminescence technique for NO detection. In addition, nasal airway resistances (NAR) were estimated by a rhinomanometer, and minimum cross-section area (MCA) and nasal cavity volume (NCV) were estimated by an acoustic rhinometer. After these estimations, 12 subjects received naphazoline nitrate 15 micrograms per nostril, and the other 12 subjects received salbutamol sulfate 100 micrograms per nostril. Finally, after 15 minutes rest, these four parameters were reviewed. The results demonstrated that naphazoline significantly decreased NO concentration and NAR, and increased NCV. Furthermore, salbutamol significantly increased NO concentration and NAR, and decreased MCA and NCV. The changes in NAR, MCA and NCV indicated that nasal mucosa became contracted and swollen by topical naphazoline and salbutamol application. Naphazoline, a nasal decongestant, contract nasal vessels by stimulating alpha 1-adrenoceptors, whereas salbutamol dilates then by stimulating beta 2-adrenoceptors, and this vasodilation does not intervene NO and cyclic GMP. Thus, nasal NO concentration is significantly affected by the change of blood supply caused simply by vasocontraction and vasodilation. In conclusion, it appeared that nasal NO concentration was possibly altered by the change of nasal blood supply, moreover, by the change in the supply of NO substrate.
Kai
T
T
Second Department of Otorhinolaryngology, Toho University School of Medicine, Tokyo.
D000281:Administration, Intranasal; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D000328:Adult; D000420:Albuterol / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D006801:Humans; D008297:Male; D009278:Naphazoline / Q000008:administration & dosage / Q000494:pharmacology; D009296:Nasal Cavity / Q000098:blood supply / Q000378:metabolism*; D014663:Nasal Decongestants / Q000008:administration & dosage / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D014663:Nasal Decongestants; D009569:Nitric Oxide; D009278:Naphazoline; D000420:Albuterol