Planta Med 2015; 81(15): 1375-1381
DOI: 10.1055/s-0035-1557775
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Dihydrogoniothalamin, an Endothelium and NO-Dependent Vasodilator Drug Isolated from Aniba panurensis

Bruno A. Rezende
1   Department of Physiology and Biophysics Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
2   Post-graduate Institute, Medical Sciences College, Belo Horizonte, MG, Brazil
,
Grazielle C. Silva
1   Department of Physiology and Biophysics Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
,
Rodrigo G. Corradi
2   Post-graduate Institute, Medical Sciences College, Belo Horizonte, MG, Brazil
,
Maria Madalena R. S. Teles
3   Laboratory of Pharmaceutical Sciences, Universidade Federal da Paraíba, João Pessoa, PB, Brazil
,
José Maria Barbosa-Filho
3   Laboratory of Pharmaceutical Sciences, Universidade Federal da Paraíba, João Pessoa, PB, Brazil
,
Virginia S. Lemos
1   Department of Physiology and Biophysics Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
,
Steyner F. Cortes
4   Department of Pharmacology, Institute of Biological Sciences. Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil
› Author Affiliations
Further Information

Publication History

received 02 March 2015
revised 26 May 2015

accepted 29 June 2015

Publication Date:
07 August 2015 (online)

Abstract

Dihydrogoniothalamin is a styrylpyrone isolated from the leaves of Aniba panurensis. The present work aimed at investigating the vasorelaxant activity of dihydrogoniothalamin and its underlying mechanism of action in the rat aorta. Dihydrogoniothalamin (0.01–100 µM) induced a concentration-dependent vasodilatation of aortas precontracted with phenylephrine. Endothelium removal or pretreatment of the preparation with NG nitro-L-arginine-methyl-ester abolished the vasodilator response for dihydrogoniothalamin. Pretreatment with calmidazolium did not affect the vasodilator response of dihydrogoniothalamin. On the other hand, wortmannin, a nonselective inhibitor of phosphatidylinositol 3-kinases, and protein kinase B inhibitor IV significantly shifted the concentration-response curve of dihydrogoniothalamin to the right and reduced its maximal effect. A nonselective antagonist of estrogen receptors, ICI 182,780, and a selective antagonist of estrogen receptor α, methyl-piperidino-pyrazole, were able to reduce the relaxation induced by dihydrogoniothalamin, but no effect was observed in the presence of the selective antagonists of estrogen receptor β and G protein-coupled receptor 30, 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol (PHTPP), and G-15, respectively. Dihydrogoniothalamin also increased the phosphorylation of the activation sites of endothelial nitric oxide synthase and protein kinase B. The present results led us to conclude that dihydrogoniothalamin is a vasodilator drug acting in an endothelium- and nitric oxide-dependent manner through a mechanism involving the activation of nitric oxide synthase via the phosphatidylinositol 3-kinase/protein kinase B pathway, partially by stimulation of estrogen receptor α.

Supporting Information

 
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