Key result
Artemisinin administration in spontaneously hypertensive rats decreased heart rate and improved endothelium-dependent vascular relaxation without significantly affecting arterial blood pressure.
Why the study?
Endothelial dysfunction characterizes hypertension, and artemisinin protects against endothelial injury in cardiac and pulmonary diseases, but its effects on vascular relaxation and blood pressure in hypertension required investigation.
Does artemisinin improve endothelium-dependent vascular relaxation and arterial blood pressure in spontaneously hypertensive rats?
Does artemisinin improve endothelium-dependent vascular relaxation and arterial blood pressure in spontaneously hypertensive rats?
Artemisinin improves endothelium-dependent vascular relaxation in hypertensive rats by modulating eNOS and NAD(P)H oxidase pathways, suggesting potential vascular protective effects.
PURPOSE: Endothelial dysfunction and the subsequent decrease in endothelium-dependent vascular relaxation of small arteries are major features of hypertension. Artemisinin, a well-known antimalarial drug, has been shown to exert protecting roles against endothelial cell injury in cardiac and pulmonary vascular diseases. The current study aimed to investigate the effects of artemisinin on endothelium-dependent vascular relaxation and arterial blood pressure, as well as the potential signalling pathways in spontaneously hypertensive rats (SHRs). METHODS: In this study, acetylcholine (ACh)-induced dose-dependent relaxation assays were performed to evaluate vascular endothelial function after treatment with artemisinin. Artemisinin was administered to the rats by intravenous injection or to arteries by incubation for the acute exposure experiments, and it was administered to rats by intraperitoneal injection for 28 days for the chronic experiments. RESULTS: Both acute and chronic administration of artemisinin decreased the heart rate and improved ACh-induced endothelium-dependent relaxation but negligibly affected the arterial blood pressure in SHRs. Incubation with artemisinin decreased basal vascular tension, NAD(P)H oxidase activity and reactive oxygen species (ROS) levels, but it also increased endothelial nitric oxide (NO) synthase (eNOS) activity and NO levels in the mesenteric artery, coronary artery, and pulmonary artery of SHRs. Artemisinin chronic administration to SHRs increased the protein expression of eNOS and decreased the protein expression of the NAD(P)H oxidase subunits NOX-2 and NOX-4 in the mesenteric artery. CONCLUSION: These results indicate that treatment with artemisinin has beneficial effects on reducing the heart rate and basal vascular tension and improving endothelium-dependent vascular relaxation in hypertension, which might occur by increasing eNOS activation and NO release and inhibiting NAD(P)H oxidase derived ROS production.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2021) studied Primary Hypertension. Artemisinin was evaluated on Endothelium-dependent vascular relaxation and arterial blood pressure. Artemisinin administration in spontaneously hypertensive rats decreased heart rate and improved endothelium-dependent vascular relaxation without significantly affecting arterial blood pressure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: