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

• Published in: Marine drugs 2011-10, Vol.9 (10), p.2075-2088
• Main Authors: Queiroz, Thyago M, Machado, Natália T, Furtado, Fabíola F, Oliveira-Filho, Abrahão A, Alustau, Maria C, Figueiredo, Camila S, Miranda, George E C, Barbosa-Filho, José M, Braga, Valdir A, Medeiros, Isac A
• Format: Article
• Language: English
• Subjects: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology; 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology; Animals; Biological Products - pharmacology; calcium; Calcium Channel Blockers - pharmacology; Calcium Channels - drug effects; Dose-Response Relationship, Drug; hypotension; Male; mesenteric artery; Muscle, Smooth, Vascular - drug effects; Phaeophyceae - chemistry; Phenylephrine - pharmacology; Potassium Chloride - pharmacology; Rats; Rats, Wistar; Tetraethylammonium - pharmacology; vasodilatation; Vasodilation - drug effects; Vasodilator Agents - pharmacology
• ISSN: 1660-3397; 1660-3397
• DOI: 10.3390/md9102075

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, CH(2)Cl(2)/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 μg/mL) from Dictyota pulchella induced a concentration-dependent relaxation in phenylephrine (Phe, 1 μM)-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 CaCl(2)-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 Ca(2+) 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.