Beta(3)-adrenoceptors control Cl(-) conductance in rabbit nasal epithelium.

We have investigated the effects of beta(3)-adrenoceptor stimulation in vivo on nasal epithelium. We have recorded the transepithelial potential difference in New Zealand white rabbit nostrils. Superfusion of the nasal epithelial surface with a Cl(-)-free medium supplemented with amiloride, hyperpolarized the nasal potential difference. Isoprenaline produced a hyperpolarization of the nasal potential difference that was not prevented by nadolol, a potent beta(1)-/beta(2)-adrenoceptor antagonist, but was abolished by bupranolol, a nonselective beta(1-3)-adrenoceptor antagonist. SR 58611 ((RS)-N-[(25)-7-ethoxycarbonylmethoxy-1,2,3,4-tetrahydronapht-2-yl]-(2R)-2-(3-chlorophenyl)-2 hydroethanamine hydrochloride) and CGP 12177 (4-[3-t-butylamino-2-hydroxypropoxy]benzimidazol-2-1), a preferential and a partial beta(3)-adrenoceptor agonists, respectively, also produced hyperpolarization of the nasal potential difference. SR 59230 (3-(2-ethylphenoxy)-1-[(1S)1,2,3,4-tetrahydronaphth-1-ylaminol]-(2S)-2-propanol oxalate), a selective beta(3)-adrenoceptor antagonist, abolished the effects of CGP 12177. We conclude that beta(3)-adrenoceptor stimulation resulted in modifications in the nasal potential difference. These findings strengthen the view that beta(3)-adrenoceptors are implicated in controlling water and salt transport in the normal respiratory epithelium.