Skip main navigation

Aging is associated with an endothelial dysfunction, which promotes cardiovascular diseases. Physical exercise has beneficial effects on the endothelial function. However, the effect of an enriched environment (EE) promoting physical exercise, on the endothelial function has not been explored during aging. We investigated the endothelial dysfunction in Long-Evans female rats housed in standard conditions (SD, 2 rats per cage) until the age of 18 months. Then, half the rats were transferred to EE (12 rats in one large cage containing various objects, which were changed 5 times per week) for 6 months. A group of 2-month old rats served as young controls. Systolic (SBP), diastolic (DBP) blood pressure and heart rate (HR) were determined by plethysmography. Vascular reactivity was assessed in mesenteric arteries using organ chambers, vascular oxidative stress by dihydroethidine staining, and the proteins expression by immunofluorescence. Aging under SD was associated with increased SBP (by 40 mmHg, P<0.001), DBP (by 12 mmHg, P<0.001) and HR (by 110 bpm, P<0.001) compared to young rats. It was also associated with blunted acetylcholine (ACh)-induced endothelium-dependent nitric oxide (NO)-mediated relaxations (EC50 1.08 10-8 M vs. 3.08 10-8 M, P<0.05) and endothelium-derived hyperpolarization (EDH)-mediated relaxation (Emax 89.5±11.8% vs. 0.28±0.18%, P<0.001), and the induction of endothelium-dependent contractile responses to ACh (Emax 0.004±0.008 g vs. 0.71±0.07 g, P<0.001) in mesenteric artery rings. EE reduced SBP and DBP by 18 and 10 mmHg, respectively (P<0.05), HR by 30 bpm (P>0.05), and improved NO-mediated responses to a similar level as in young rats (P<0.001) without affecting the blunted EDH-mediated relaxation and the increased endothelium-dependent contractile responses in old rats. An excessive oxidative stress and the upregulation of endothelial NO synthase (eNOS), nitrotyrosine and arginase I were observed in the aorta of SD old rats compared to young rats (P<0.001). EE improved all these effects (P<0.05). In conclusion, EE retarded the aging-related endothelial dysfunction mostly by improving the NO-mediated relaxation. This effect involves normalization of vascular oxidative stress and possibly also eNOS uncoupling.


eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.

Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.