Vasorelaxation, Induced by Dictyota pulchella (Dictyotaceae), a Brown Alga, Is Mediated via Inhibition of Calcium Influx in Rats

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 pulchella produced dose-dependent hypotension (-4 +/- 1; -8 +/- 2; -53 +/- 8 and -63 +/- 3 mmHg) and bradycardia (-8 +/- 6; -17 +/- 11; -257 +/- 36 and -285 +/- 27 b.p.m.). In addition, CME and Hexane/EtOAc Phase (HEP) (0.01-300 mu g/mL) from Dictyota pulchella induced a concentration-dependent relaxation in phenylephrine (Phe, 1 mu M)-pre-contracted mesenteric artery 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 A(2) agonist U-46619 (100 nM). Furthermore, CME and HEP reversed CaCl2-induced vascular contractions. These results suggest that both CME and HEP act on the 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 Ca2+ influx through blockade of voltage-operated calcium channels.