Vasorelaxation, induced by Dictyota pulchella (Dictyotaceae), a brown alga,is mediated via inhibition of calcium influx in rats

Abstract

This study aimed to investigate the cardiovascular effects elicited by Dictyota pulchella, a brown alga, using in vivo and in vitro approaches. In normotensive conscious rats, CH2Cl2/MeOH Extract (CME, 5, 10, 20 and 40 mg/kg) from Dictyota pulchellaproduced dose-dependent hypotension (-4 ± 1; -8 ± 2; -53 ± 8 and -63 ± 3 mmHg) andbradycardia (-8 ± 6; -17 ± 11; -257 ± 36 and -285 ± 27 b.p.m.). In addition, CME andHexane/EtOAc Phase (HEP) (0.01-300 μg/mL) from Dictyota pulchella induced aconcentration-dependent relaxation in phenylephrine (Phe, 1 μM)-pre-contracted mesentericartery rings. The vasorelaxant effect was not modified by the removal of the vascular endothelium or pre-incubation with KCl (20 mM), tetraethylammonium (TEA, 3 mM) or tromboxane A2 agonist U-46619 (100 nM). Furthermore, CME and HEP reversedCaCl2-induced vascular contractions. These results suggest that both CME and HEP act onthe voltage-operated calcium channel in order to produce vasorelaxation. In addition, CME induced vasodilatation after the vessels have been pre-contracted with L-type Ca2+channel agonist (Bay K 8644, 200 nM). Taken together, our data show that CME induces hypotension and bradycardia in vivo and that both CME and HEP induce endothelium-independent vasodilatation in vitro that seems to involve the inhibition of the Ca 2+ influx through blockade of voltage-operated calcium channels. © 2011 by the authors; licensee MDPI.