Key result
Prunetin lowers SBP by ~36 mmHg in hypertensive rats by blocking calcium channels.
Why the study?
Does prunetin induce vasorelaxation and reduce blood pressure in rat models?
Does prunetin induce vasorelaxation and reduce blood pressure in rat models?
Mean Difference: -36
Absolute Event Rate: 183% vs 222.3%
p-value: p=<0.01
Prunetin demonstrates vasorelaxant and hypotensive effects in rat models by blocking calcium channels.
Should not change clinical practice; hypothesis-generating for prunetin in human hypertension.
Prunetin, a component of herbal medicines and various foods, such as pea, peach, cherry, and Prunus yedoensis, is a useful pharmacological compound. We previously reported the potent vasorelaxant effect of the bark of P. yedoensis. Therefore, we investigated the vasorelaxant activities of prunetin on isolated rat aortic rings and hypotensive activity on spontaneously hypertensive rats (SHR) in this study. In the present study, prunetin (1–30 μg/mL) relaxed isolated rat aortic rings pre-contracted by phenylephrine (PE) in a concentration-dependent manner. Pre-incubation with prunetin (3 and 10 μg/mL) inhibited vasoconstriction induced by the supply of Ca2+ in rat aortic rings pre-contracted with PE or KCl in a Ca2+-free Krebs–Henseleit (KH) buffer. Prunetin (10 μg/mL) pre-treatment also inhibited caffeine-induced contraction of aortic rings in a Ca2+-free KH buffer. To investigate the hypotensive effect of prunetin, the systolic blood pressure (SBP) of the SHR was measured by using a tail cuff assay. The SBP of SHR was significantly lower in the prunetin (25 mg/kg)-treated group. These results suggested that prunetin decreased blood pressure and relaxed blood vessels by blocking receptor-operated calcium channels, voltage-dependent calcium channels, and ryanodine receptor channels.
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Kim et al. (2018) studied Hypertension (n=12). Prunetin vs. Distilled water was evaluated on Systolic blood pressure (SBP) at 4 hours (MD -36.0 mmHg, p=<0.01). Prunetin significantly decreased systolic blood pressure in spontaneously hypertensive rats by 36.0 mmHg at 4 hours post-administration and induced vasorelaxation by blocking calcium channels.
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