摘要
Objective To study the effects of anisodamine on microvessels and its relationship with endothelium target for acetylcholine (ETA). Methods Norepinephrine precontracted mesen-teric vascular beds in rat were used to determine changes of tension of vessels in response to anisodamine after removal of endotlielium, coincubated with L- NAME, nitric oxide synthase (NOS ) inhibitor, in-domethacin,cyclo-oxygenase inhibitor and glibenclamide, ATP-dependent K+ channels (KATP) inhibitor. Results Anisodamine produced a vasodilatian effect on mesenteric vascular beds,which was remarkably inhibited after removal of endothelium (P<0. 01). The vasodilation effect of anisodamine was also significantly inhibited after coincubated with indometliacin (1 μmol/U) ,NG-nitro-L-arginine methyl ester (L-NAME,100 μmol/L) and glibenclamide (1 /μmol/L, P< 0. 01, vs control). Conclusion The vasodilation effect of anisodamine on microvessels was mediated by ETA. This is related to prostacyclin,endothelium derived relaxing factor (EDRF) and KATP besides M, a-receptor on vascular smooth muscle cell(VSMC) and calcium-antagonistic effects.
Objective To study the effects of anisodamine on microvessels and its relationship with endothelium target for acetylcholine (ETA). Methods Norepinephrine precontracted mesen-teric vascular beds in rat were used to determine changes of tension of vessels in response to anisodamine after removal of endotlielium, coincubated with L- NAME, nitric oxide synthase (NOS ) inhibitor, in-domethacin,cyclo-oxygenase inhibitor and glibenclamide, ATP-dependent K+ channels (KATP) inhibitor. Results Anisodamine produced a vasodilatian effect on mesenteric vascular beds,which was remarkably inhibited after removal of endothelium (P<0. 01). The vasodilation effect of anisodamine was also significantly inhibited after coincubated with indometliacin (1 μmol/U) ,NG-nitro-L-arginine methyl ester (L-NAME,100 μmol/L) and glibenclamide (1 /μmol/L, P< 0. 01, vs control). Conclusion The vasodilation effect of anisodamine on microvessels was mediated by ETA. This is related to prostacyclin,endothelium derived relaxing factor (EDRF) and KATP besides M, a-receptor on vascular smooth muscle cell(VSMC) and calcium-antagonistic effects.
基金
Supported by National 973 Project (G1998051112)
