The Journal of pharmacy and pharmacology · 2026
Acute intravenous antihypertensive and in vitro vasorelaxant effect of the hydroalcoholic stem bark extract of Hymenaea rubriflora Ducke in spontaneously hypertensive rats.
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Toscano Luciana Tavares, Moraes Milton Rocha, Veras Robson Cavalcante, Maciel Priscilla Maria Pereira, Assis Kívia Sales, Lima Franciely Oliveira, Júnior Jayme César Silva, de Magalhães Cordeiro Angela Maria Tribuzy, Medeiros Isac Almeida, Dos Santos Rosa Thiago, Silva Alexandre Sérgio
Аннотация
OBJECTIVES: The cardioprotective potential of Hymenaea rubriflora Ducke's stem bark hydroalcoholic extract (HR-HAc) has not yet been investigated. This study aimed to quantify HR-HAc's antioxidant capacity and evaluate its effects on blood pressure (BP) and vascular reactivity in spontaneously hypertensive rats (SHR).
METHODS: SHR and normotensive Wistar Kyoto (WKY) rats received intravenous HR-HAc (2.5-60 mg/kg). Mean arterial pressure (MAP) and heart rate (HR) were measured with or without atropine and propranolol. Isolated aortas from SHR and WKY rats were exposed to HR-HAc (0.1-729 μg/ml), with or without endothelium and K+ channel blockers. Phenolic content and antioxidant activity were quantified using standard colorimetric and chromatographic methods.
KEY FINDINGS: In SHR rats, HR-HAc produced dose-dependent hypotension and bradycardia. MAP reduction in WKY rats was similar, while HR was unaffected. Atropine significantly attenuated HR-HAc-induced reductions in MAP and HR in SHR rats. HR-HAc induced potent endothelium-independent relaxation in SHR rat aortas, which was significantly reduced by tetraethylammonium or 4-aminopyridine. In WKY rats, vasorelaxant effects were endothelium-dependent.
CONCLUSIONS: HR-HAc lowers MAP and induces bradycardia in SHR via muscarinic receptors, while also promoting vasodilation through activation of voltage- and calcium-activated K+ channels. These distinct mechanisms highlight HR-HAc as a promising preclinical antihypertensive candidate.
METHODS: SHR and normotensive Wistar Kyoto (WKY) rats received intravenous HR-HAc (2.5-60 mg/kg). Mean arterial pressure (MAP) and heart rate (HR) were measured with or without atropine and propranolol. Isolated aortas from SHR and WKY rats were exposed to HR-HAc (0.1-729 μg/ml), with or without endothelium and K+ channel blockers. Phenolic content and antioxidant activity were quantified using standard colorimetric and chromatographic methods.
KEY FINDINGS: In SHR rats, HR-HAc produced dose-dependent hypotension and bradycardia. MAP reduction in WKY rats was similar, while HR was unaffected. Atropine significantly attenuated HR-HAc-induced reductions in MAP and HR in SHR rats. HR-HAc induced potent endothelium-independent relaxation in SHR rat aortas, which was significantly reduced by tetraethylammonium or 4-aminopyridine. In WKY rats, vasorelaxant effects were endothelium-dependent.
CONCLUSIONS: HR-HAc lowers MAP and induces bradycardia in SHR via muscarinic receptors, while also promoting vasodilation through activation of voltage- and calcium-activated K+ channels. These distinct mechanisms highlight HR-HAc as a promising preclinical antihypertensive candidate.