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Abstract
This investigation was aimed to provide pharmacological evidences for the medicinal use of Capparis aphylla in hypertension. In normotensive anesthetized rats, intravenous administration of the crude extract of Capparis aphylla (Ca.Cr; 3–100 mg/kg) caused a fall in mean arterial pressure (MAP), which was partially blocked in the presence of atropine (2 mg/kg). In isolated rabbit aortic rings, Ca.Cr inhibited phenylephrine (1 μM) and high K+ (80 mM) precontractions with respective EC50 values of 0.10 (0.07–0.15) and 1.22 mg/mL (1.00–1.50), suggesting calcium channel blocking (CCB) activity with a predominant inhibitory effect on receptor operated Ca2+ channels. Pretreatment of the arotic rings with Ca.Cr (0.1–1 mg/mL) caused a rightward shift in the Ca2+ concentration response curves, similar to verapamil. In isolated rat aorta preparations, Ca.Cr caused a partial endothelium-dependent L-NAME/atropine-sensitive vasodilator effect. In guinea-pig atria, Ca.Cr suppressed both rate and force of spontaneous atrial contractions with respective EC50 values of 1.35 (1.01–1.79) and 1.60 mg/mL (1.18–2.17), which remained unchanged in the presence of atropine (1 μM). These data indicate that the blood pressure (BP) lowering effect of the crude extract of Capparis aphylla is mediated through a vasodilator and cardiac depressant effect. The vasodilator effect is partly mediated by an endothelium-dependent, atropine-sensitive NO pathway, while the CCB effect is partly responsible for endothelium-independent vasodilatation and also for the cardiac depressant effect; thus, this study provides pharmacologic evidence with respect to the medicinal use of the plant in hypertension.
ACKNOWLEDGMENT
This study was supported in part by the Pakistan Science Foundation.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.