Blood pressure-lowering and vascular modulator effects of Acorus calamus extract are mediated through multiple pathways.
This investigation was aimed to provide a pharmacologic basis to the medicinal use of Acorus calamus in cardiovascular disorders. In normotensive anesthetized rats, crude extract of Acorus calamus and its ethylacetate and nHexane fractions caused a fall in mean arterial pressure. In rabbit aorta rings, crude extract was more potent against high K (80 mM), ethylacetate against phenylephrine (1 microM), whereas nHexane fraction was equipotent against both precontractions. Crude extract exhibited a vasoconstrictor effect on baseline. Pretreatment of aortic rings with crude extract and its fractions shifted Ca concentration-response curves to the right, similar to verapamil. Crude extract and ethylacetate fraction suppressed phenylephrine peak formation in Ca-free medium. In rat aorta preparations, crude extract exhibited endothelium-independent relaxation with a vasodilatory effect against high K. nHexane fraction caused an endothelium-dependent Nomega-nitro-l-arginine methyl ester-sensitive vasorelaxant along with ryanodine-sensitive vasoconstrictor effect on baseline tension and partially inhibited high K, although ethylacetate fraction caused an endothelium-independent relaxant and endothelium-dependent vasoconstrictor effect. These data indicate that crude extract possesses a combination of effects, relaxant effects mediated possibly through Ca antagonism in addition to a nitric oxide pathway, although the associated vasoconstrictor effects may be meant by nature to offset excessive vasodilatation, thus providing a pharmacologic rationale to its cardiovascular medi-cinal uses.
Shah
Abdul Jabbar
AJ
Drug Discovery and Natural Products Research Division, Department of Biological and Biomedical Sciences, Aga Khan University Medical College, Karachi-74800, Pakistan.
Gilani
Anwarul Hassan
AH
D000109:Acetylcholine / Q000494:pharmacology; D029023:Acorus / Q000033:anatomy & histology / Q000737:chemistry*; D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000378:metabolism; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D002110:Caffeine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D020128:Inhibitory Concentration 50; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010936:Plant Extracts / Q000494:pharmacology*; D018517:Plant Roots / Q000737:chemistry; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012015:Reference Standards; D012433:Ryanodine / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D014700:Verapamil / Q000494:pharmacology
D010936:Plant Extracts; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D012433:Ryanodine; D010656:Phenylephrine; D002110:Caffeine; D004533:Egtazic Acid; D011189:Potassium Chloride; D001285:Atropine; D014700:Verapamil; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine; D007213:Indomethacin