AI Article Synopsis
- The study highlights that while endothelial dysfunction is generally accepted in hypertensive models, some research shows that vasodilatory responses in spontaneously hypertensive rats (SHR) can be similar or even enhanced compared to normotensive rats.
- Factors contributing to these discrepancies include the animal's age, the specific type of artery being studied, and the methodologies used in experiments.
- Antioxidant additives and variations in initial arterial stretch may influence arterial oxidative status and the release of vasoactive factors, affecting the overall assessment of endothelial function in hypertensive conditions.
Article Abstract
Despite the apparent consensus on the existence of endothelial dysfunction in conduit and resistance arteries of spontaneously hypertensive rats (SHR), a commonly employed experimental model of hypertension, there are a number of reports showing that endothelium-dependent vasodilatory responses are similar, or even increased, in SHR compared with their normotensive counterparts. The present paper aims to discuss the rationale for these apparent discrepancies, including the effect of age, type of artery and methodological aspects. Data from the literature indicate that the age of the animal is a contributing factor and that endothelial dysfunction is likely to be a consequence of hypertension. In addition, the use of antioxidant additives, such as ascorbic acid or ethylene diaminetetraacetic acid, and differences in the level of initial arterial stretch, might also be of importance because they may modify the oxidative status of the artery and the levels of vasoactive factors released by the endothelium.
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| http://dx.doi.org/10.1097/01.hjh.0000358834.18311.fc | DOI Listing |
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