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Journal of Ethnopharmacology 2012-Mar

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats.

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
Ismaila A Raji
Pierre Mugabo
Kenechukwu Obikeze

Atslēgvārdi

Abstrakts

BACKGROUND

Tulbaghia violacea Harv. (Alliaceae) is a small bulbous herb which belongs to the family Alliaceae, most commonly associated with onions and garlic. In South Africa, this herb has been traditionally used in the treatment of various ailments, including fever, colds, asthma, paralysis, hypertension and stomach problems. The aim of this study was to evaluate the effect of methanol leaf extracts (MLE) of Tulbaghia violacea on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive rats; and to find out the mechanism(s) by which it acts.

METHODS

The MLE of Tulbaghia violacea (5-150mg/kg), angiotensin I human acetate salt hydrate (ang I, 3.1-100μg/kg), angiotensin II human (ang II, 3.1-50μg/kg), phenylephrine hydrochloride (phenylephrine, 0.01-0.16mg/kg) and dobutamine hydrochloride (dobutamine, 0.2-10.0μg/kg) were infused intravenously, while the BP and HR were measured via a pressure transducer connecting the femoral artery and the Powerlab.

RESULTS

Tulbaghia violacea significantly (p<0.01) reduced the systolic, diastolic, and mean arterial BP; and HR dose-dependently. Ang I, ang II, phenylephrine and dobutamine all increased the BP dose-dependently. The hypertensive effect of ang I and the HR-increasing effect of dobutamine were significantly (p<0.01) decreased by their co-infusion with Tulbaghia violacea (60mg/kg). However, the co-infusion of ang II or phenylephrine with Tulbaghia violacea (60mg/kg) did not produce any significant change in BP or HR when compared to the infusion of either agent alone in the same animal.

CONCLUSIONS

Tulbaghia violacea reduced BP and HR in the SHR. The reduction in BP may be due to actions of the MLE on the ang I converting enzyme (ACE) and β(1) adrenoceptors.

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