Beta-adrenergic mechanisms in the nasal mucosa vascular bed

Abstract

In thiopentone-anesthetized mature pigs (n = 7), local intra-arterial infusion of the β₂-adrenoceptor agonists terbutaline and salbutamol and the β₃-agonist BRL 37344 induced dose-dependent increases in nasal arterial blood flow (BF) and volume of the nasal mucosa (reflecting capacitance vessel function). Increases were also found in the laser Doppler flowmeter signal, reflecting superficial mucosal BE. In contrast to terbutaline and salbutamol, BRL 37344 showed marked effects on volume. Pretreatment with the β-adrenoceptor blocker propranolol significantly reduced the vasodilatory effects of terbutaline and salbutamol, whereas the BF increase evoked by BRL 37344 was not affected. Exogenous noradrenaline (NA) induced in vitro dose-dependent contractions of human nasal mucosa biopsies obtained from patients with non-allergic chronic rhinitis (n = 21) or non-allergic nasal polyposis (NANP, n = 16). On a molar basis, the contractile effect of NA was significantly greater in nasal mucosa samples without histological abnormalities when compared to biopsies with abundant inflammatory cells and edema within the submucosa. In the presence of propranolol, the vasoconstrictor effect of NA was significantly enhanced in biopsies with abundant inflammatory cells obtained from patients with NANP (P<0.01). This observation suggests the possible occurrence of a β₂ hyper-reactivity in the nasal mucosa of patients with NANP. After precontraction in a Krebs-Ringer solution with 50 nM K⁺, all nasal biopsies studied showed dose-dependent relaxation to terbutaline, salbutamol and BRL 37344. This relaxant effect was markedly reduced after pretreatment with propranolol. These observations suggest that β₂- and β₃-adrenergic vasodilatatory mechanisms may be similar in the nasal mucosa of the pig and man.