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Coronary vasodilator activity of vulgarenol, a sesquiterpene isolated from Magnolia grandiflora , and its possible mechanism
Author(s) -
ValleMondragón L. del,
TenorioLópez F. A.,
TorresNarváez J. C.,
ZarcoOlvera G.,
PastelínHernández G.
Publication year - 2009
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2696
Subject(s) - nitric oxide , cyclic guanosine monophosphate , vasodilation , guanosine , pharmacology , coronary perfusion pressure , sesquiterpene , chemistry , medicine , biochemistry , anesthesia , stereochemistry , cardiopulmonary resuscitation , resuscitation
The aim of this study was to investigate the biodynamic effects of vulgarenol, a sesquiterpene isolated from Magnolia grandiflora flower petals and its possible mechanism on the Langendorff isolated and perfused heart model. Vulgarenol (5 µ m ) caused a statistically significant decrease in coronary vascular resistance (15.21 ± 6.00 dyn s cm −5 vs 36.80 ± 5.01 dyn s cm −5 , control group), increased nitric oxide release (223.01 ± 8.76 pmol/mL vs 61.00 ± 12.00 pmol/mL, control group) and cyclic guanosine monophosphate accumulation in left ventricular tissue samples (142.17 ± 8.41 pmol/mg of tissue vs 43.94 ± 5.00 pmol/mg of tissue, control group). Pre‐treatment with 3 µ m gadolinium chloride hexahydrate, 100 µ m N ω ‐nitro‐ l ‐arginine methyl ester hydrochloride, and 10 µ m 1 H ‐[1,2,4]oxadiazolo[4,2‐ a ]quinoxalin‐1‐one significantly abolished the vulgarenol‐induced coronary vascular resistance decrease, nitric oxide increased release and cGMP accumulation in left ventricular tissue samples. The results support the fact that nitric oxide and cyclic guanosine monophosphate are likely involved in the endothelium‐dependent coronary vasodilation. Copyright © 2008 John Wiley & Sons, Ltd.