OBJECTIVETo investigate the expression and distribution of alpha1-adrenoceptor subtypes in rabbit submandibular gland and the effect of phenylephrine on salivary secretion.

METHODSThe expressions of alpha1A-, alpha1B-, and alpha1D-adrenoceptor mRNA and protein were investigated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot in rabbit submandibular gland. Immunohistochemical assay was applied to detect the distribution of alpha1A-, alpha1B-, and alpha1D-adrenoceptor and localization of aquaporin 5 in rabbit submandibular gland. Different concentrations of phenylephrine (1 x 10(-8))-(1 x 10(-6)) mol/L were administrated through a polyethylene tube, which was intubated into Wharton's duct of submandibular gland. Heart rate and blood pressure of rabbits were observed during phenylephrine administration. Salivary flow was measured by the length of moist filter paper (35 mm x 5 mm) within 5 min.

RESULTSAlpha1A-, alpha1B-, and alpha1D-adrenoceptor mRNA and protein were expressed in rabbit submandibular gland. Three alpha1-adrenoceptor subtypes were widely distributed in the membrane and cytoplasma of both acinar and ductal cells. Phenylephrine (1 x 10(-7) mol/L, 100 microl) stimulated effectively salivary secretion without inducing significant alteration of blood pressure and heart rate in rabbit. Immunohistochemical assay showed that aquaporin 5 was mainly localized in the apical and lateral plasma membrane in both acinar and ductal cells in unstimulated condition, while the expression of aquaporin 5 was increased after administration of phenylephrine.

CONCLUSIONSExpression of alpha1A-, alpha1B-, and alpha1D-adrenoceptor mRNA and protein was existed in rabbit submandibular gland. Phenylephrine safely and effectively promoted salivary secretion when it was administrated through Wharton's duct of submandibular gland. The mechanism of phenylephrine on salivary secretion may involve in the increase of expression of aquaporin 5 in the apical and lateral plasma membrane in rabbit submandibular gland. This study will hopefully lead to a novel strategy for clinical treatment of dysfunction of submandibular gland.