Electrical stimulation-induced alpha1- and alpha2-adrenoceptors-mediated contraction in isolated dog thoracic ducts.

The electrical stimulation-induced responses of isolated dog thoracic ducts were investigated using an organ bath technique. Electrical stimulation (0.7 ms in pulse width, 25 V in nominal voltage, 10 s in duration time, 1-32 Hz at frequency) produced frequency-related contractions in the lymphatic preparations. The contractions were abolished by pretreatment with tetrodotoxin (10(-7) M), guanethidine (10(-7), 10(-6) M), and bretylium (10(-7), 10(-6) M). Cocaine (10(-6) M) significantly potentiated the electrical stimulation-induced contractions. Phentolamine (10(-8)-10(-5) M), prazosin (10(-8)-10(-5) M), bunazosin (10(-6), 10(-5) M), yohimbine (10(-8)-10(-6) M) and rauwolscine (10(-8)-10(-6) M) also dose-dependently reduced the contractions. On the other hand, propranolol (10(-8)-10(-6) M), atropine (10(-6) M), hexamethonium (10(-6) M), aspirin (3 x 10(-5) M), N(omega)-nitro-L-arginine methyl ester (L-NAME) (3 x 10(-5) M) and L-NAME (3 x 10(-5) M) + L-arginine (10(-4) M) caused no significant effect on electrical stimulation-induced contractions. No significant difference in the electrical stimulation-induced responses was observed between the lymphatic preparations with and without an intact endothelium. The electrical stimulation caused only a small contraction with no relaxation in the thoracic duct preparation precontracted with 10(-8) M U46619. The small contraction was abolished by 10(-5) M phentolamine. These findings suggest that there exists alpha1- and alpha2-adrenoceptors-mediated excitatory innervation, but no NO-ergic inhibitory nerve fiber in dog thoracic ducts.