Objectives: Cleistanthins A and B are the active compounds isolated from Cleistanthus collinus leaves. The hypotensive activity of both cleistanthins A and B and the leaf extract has been previously demonstrated, but the exact mechanism of action is not clear. So, this study was designed to test the vasorelaxant property of cleistanthins A and B and delineate its mechanism of action. Methods: Variable force transducers were used to record the force of contraction from the aortic rings of 24 male guinea pigs. The effect of cleistanthin A, cleistanthin B, prazosin and vehicle on the phenylephrine-induced contractions and potassium chloride-induced contractions was demonstrated and compared. Results: Cleistanthin B inhibited the phenylephrine-induced contractions in a dose-dependent manner and demonstrated potency (pIC50 = 6.8 ± 1.06) comparable to prazosin (pIC50 = 5.7 ± 0.7). Cleistanthin A potency could not be calculated. Both cleistanthin A (4 μg) and cleistanthin B (40 μg) caused a reduction of the maximal response of phenylephrine demonstrating irreversible blockade. They did not affect the potassium chloride-induced contractions. This illustrates that cleistanthins A and B are noncompetitive α1 adrenergic blockers and the potency of cleistanthin B is comparable to prazosin. Conclusion: Both cleistanthins A and B have vasodilatory action on guinea pig aorta. The action is through non-competitive α1 adrenergic receptor inhibition and calcium channel blockade does not contribute to the inhibition.
Key words: α1 adrenergic antagonist, Cleistanthin A, Cleistanthin B, Cleistanthus collinus, Guinea pig, Isolated aortic rings.