Possible mechanisms of action of the hypotensive effect of Annona muricata (soursop) in normotensive Sprague-Dawley rats

Context: Annona muricata Linn (Annonaceae) (soursop) is a food plant reported to have antihypertensive properties. Objective: We investigated the blood pressure reducing effect of its aqueous leaf extract and the possible mechanisms that may be responsible. Methods: Intravenous administration of an...

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Veröffentlicht in:Pharmaceutical biology 2012-11, Vol.50 (11), p.1436-1441
Hauptverfasser: Nwokocha, Chukwuemeka R., Owu, Daniel U., Gordon, Angeline, Thaxter, Karen, McCalla, Garsha, Ozolua, Raymond I., Young, Lauriann
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Sprache:eng
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Zusammenfassung:Context: Annona muricata Linn (Annonaceae) (soursop) is a food plant reported to have antihypertensive properties. Objective: We investigated the blood pressure reducing effect of its aqueous leaf extract and the possible mechanisms that may be responsible. Methods: Intravenous administration of an aqueous leaf extract (9.17-48.5 mg/kg) of A. muricata on the mean arterial pressure and heart rate were recorded invasively on anaesthetized, normotensive Sprague-Dawley rats. Contractile responses of rat aortic rings to the extract (0.5-4.0 mg/mL) were studied using standard organ bath techniques. Results: A. muricata (9.17-48.5 mg/kg) caused significant (p < 0.05) dose-dependent reduction in blood pressure without affecting the heart rates. The hypotensive effects were unaffected by atropine (2 mg/kg), mepyramine (5 mg/kg), propranolol (1 mg/kg) and L-NAME (5 mg/kg). A. muricata leaf aqueous extract significantly (p < 0.05) relaxed phenylephrine (10−9-10−4 M) and 80 mM KCl induced contractions in endothelium intact and denuded aortic rings; and caused a significant (p < 0.05) rightward shift of the Ca2+ dose response curves in Ca2+-free Kreb's solution containing 0.1 mM EGTA. Conclusions: The hypotensive effects of A. muricata are not mediated through muscarinic, histaminergic, adrenergic and nitric oxide pathways, but through peripheral mechanisms involving antagonism of Ca2+.
ISSN:1388-0209
1744-5116
DOI:10.3109/13880209.2012.684690