New C(28) steroidal glycosides from Tubocapsicum anomalum.

Two new C(28) steroidal glycosides, tuboanosides A (1) and B (2), were isolated from the fruit of Tubocapsicum anomalum MAKINO. Their chemical structures were elucidated on the basis of spectroscopic and X-ray diffraction analysis of the p-bromobenzoyl derivative (4) of tuboanosigenin (3), the sapogenol derivative of these two glycosides. Tuboanosides have the structural peculiarity of an unusual side chain carrying an unusual linkage with a C-21 bound to C-25 on the lactone ring.

[Studies on antihypertensive effect of Luobuma (Apocynum venetum L.) leaf extract (3)].

To clarify the mechanisms underlying the antihypertensive effect of Luobuma (Apocynum venetum L. (Apocynaceae)) leaf extract (LLE), we investigated the vasodilator effect of LLE in the rat mesenteric vascular bed, which plays an important role in changes in peripheral resistance and thus the regulation of blood pressure. In the perfused mesenteric vascular bed with active tone and intact endothelium, perfusion of LLE (0.1 ng to 100 mg/ml for 15 min) caused dose-dependent vasodilation, which was abolished by chemical removal of the endothelial layer with perfusion of sodium deoxycholate, but not by N(G)-nitro-L-arginine-methyl ester (L-NAME), a competitive inhibitor of nitric oxide (NO), which instead increased the effect. The LLE-induced vasodilation was partially inhibited by high K(+)-containing Krebs solution and tetraethylammonium (a K(+) channel blocker) and completely by the combination of L-NAME and high K(+)-Krebs solution. However, atropine (a muscarinic acetylcholine receptor antagonist) did not affect the vasodilation. These results suggest that the vasodilation induced by LLE is endothelium-dependent and mediated by endothelium-derived hyperpolarizing factor, which involves the activation of K(+)-channels. The higher concentrations of LLE may enhance NO production/release to cause vasodilation.