Action of dauricine on aortic strips
Abstract
Dauricine (Dau) inhibited both the contractions evoked by Adr or high K+ in rabbit thoracic aortic strips and those caused by NA in normal or hypertensive rat aortic strips.
It shifted the dose-response curves for NA, KCI and CaCl2 to the right, and depressed their maximal responses.
Dau produced neitherα-adrenoceptic bloking norβ-adrenoceptic stimulating effects.
It antagonized NA and Ca2+ in a non-competitive manner. The antagonism of Dau against NA was as potent as that of verapamil (Ver), but it was much weaker than Ver against Ca2+.
Dau inhibited both the fast and transitory contraction (Cai2+-dependent) responses evoked by NA in Ca2+-free medium and the slow sustained contraction (Ca02+-dependent) response after the supplement of CaCl2. On the contrary, Ver inhibited the fast and transitory contraction response, but not the slow sustained contraction response.
These results suggested that the Dau-induced relaxation on vascular smooth muscle might result from its antagonistic effect to Ca2+ and that the mode of this antagonism differed from that of Ver. It is possible that these 2 drugs interfere with 2 different transmembrane Ca2+ channels.
Keywords:
It shifted the dose-response curves for NA, KCI and CaCl2 to the right, and depressed their maximal responses.
Dau produced neitherα-adrenoceptic bloking norβ-adrenoceptic stimulating effects.
It antagonized NA and Ca2+ in a non-competitive manner. The antagonism of Dau against NA was as potent as that of verapamil (Ver), but it was much weaker than Ver against Ca2+.
Dau inhibited both the fast and transitory contraction (Cai2+-dependent) responses evoked by NA in Ca2+-free medium and the slow sustained contraction (Ca02+-dependent) response after the supplement of CaCl2. On the contrary, Ver inhibited the fast and transitory contraction response, but not the slow sustained contraction response.
These results suggested that the Dau-induced relaxation on vascular smooth muscle might result from its antagonistic effect to Ca2+ and that the mode of this antagonism differed from that of Ver. It is possible that these 2 drugs interfere with 2 different transmembrane Ca2+ channels.