Calcium channel blocking activity of calycosin, a major active component of Astragali Radix, on rat aorta.
OBJECTIVE
To investigate the vasoactivity of calycosin, a major active component of Astragali Radix.


METHODS
Experiments were performed on isolated rat thoracic aortic rings pre-contracted with phenylephrine (PHE) or KCl.


RESULTS
Calycosin produced a concentration-dependent relaxation on the tissue pre-contracted using PHE with 4.46+/-0.13 of pD(2) and 95.85%+/-2.67% of E(max); or using KCl with 4.27+/-0.05 of pD2 and 99.06%+/-2.15% of Emax, and displaced downwards the concentration-response curves of aortic rings to PHE or KCl. The relaxant effect of calycosin on denuded endothelium aortic rings was the same as on intact endothelium aortic rings, and its vasorelaxant effect was not influenced by L-NAME or indomethacin. In Ca(2+)-free solution, calycosin (30 micromol/L) did not have an effect on PHE (1 micromol/L)-induced aortic ring contraction. The effects of calycosin and nifedipine where somewhat different; calycosin decreased aortic ring contractions induced by the two agonists, but nifedipine displayed a more potent inhibitory effect on KCl-induced contractions than on PHE-induced contractions, and the vascular relaxing effects of calycosin and nifidipine were additive on PHE-induced contraction but not KCl-induced.


CONCLUSIONS
Calycosin is a vasorelaxant. Its action is endothelium-independent and is unrelated to intracellular Ca(2+) release. It is a noncompetitive Ca(2+) channel blocker. The effect of calycosin on Ca(2+) channel blockade may be different from that of dihydropyridines. This study demonstrated a novel pharmacological activity of calycosin, and supplied a theoretic foundation for Astragali Radix application.
Wu
Xiu-Li
XL
Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University, Beijing 100083, China.
Wang
Yin-Ye
YY
Cheng
Jun
J
Zhao
Yu-Ying
YY
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D027885:Astragalus propinquus / Q000737:chemistry; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002122:Calcium Chloride / Q000037:antagonists & inhibitors; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology; D007529:Isoflavones / Q000302:isolation & purification / Q000494:pharmacology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009543:Nifedipine / Q000494:pharmacology; D010656:Phenylephrine / Q000037:antagonists & inhibitors; D018517:Plant Roots / Q000737:chemistry; D010946:Plants, Medicinal / Q000737:chemistry; D011189:Potassium Chloride / Q000037:antagonists & inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D014665:Vasodilator Agents / Q000494:pharmacology*
D002121:Calcium Channel Blockers; D007529:Isoflavones; D014665:Vasodilator Agents; C121707:7,3'-dihydroxy-4'-methoxyisoflavone; D010656:Phenylephrine; D011189:Potassium Chloride; D009543:Nifedipine; D002122:Calcium Chloride; D002118:Calcium