Endothelial dysfunction in experimental models of arterial hypertension appears to be a consequence of high blood pressure rather than its cause, driven by an imbalance in endothelium-derived factors.
This review suggests that in experimental models of hypertension, endothelial dysfunction is typically a consequence of high blood pressure rather than its primary cause.
Hypertension is a risk factor for other cardiovascular diseases and endothelial dysfunction was found in humans as well as in various commonly employed animal experimental models of arterial hypertension. Data from the literature indicate that, in general, endothelial dysfunction would not be the cause of experimental hypertension and may rather be secondary, that is, resulting from high blood pressure (BP). The initial mechanism of endothelial dysfunction itself may be associated with a lack of endothelium-derived relaxing factors (mainly nitric oxide) and/or accentuation of various endothelium-derived constricting factors. The involvement and role of endothelium-derived factors in the development of endothelial dysfunction in individual experimental models of hypertension may vary, depending on the triggering stimulus, strain, age, and vascular bed investigated. This brief review was focused on the participation of endothelial dysfunction, individual endothelium-derived factors, and their mechanisms of action in the development of high BP in the most frequently used rodent experimental models of arterial hypertension, including nitric oxide deficient models, spontaneous (pre)hypertension, stress-induced hypertension, and selected pharmacological and diet-induced models.
Iveta Bernátová (Wed,) conducted a review in Arterial hypertension. Endothelial dysfunction was evaluated. Endothelial dysfunction in experimental models of arterial hypertension appears to be a consequence of high blood pressure rather than its cause, driven by an imbalance in endothelium-derived factors.