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- Title
F006: Age-related endothelial dysfunction is prevented by physical activity.
- Authors
Salvetti, G.; Ciuti, F.; Virdis, A.; Ghiadoni, L.; Galetta, F.; Franzoni, F.; Taddei, S.; Salvetti, A.
- Abstract
Aging is a cardiovascular risk factor characterized by an impaired endothelium (END)-dependent vasodilation (VD) caused by a reduced nitric oxide (NO) availability due to oxidative stress. Aim of the study was to evaluate whether this alteration could be prevented by physical activity. In 14 normotensive elderly athletes (EA, long runners: age 65.3 ± 8.2, range 51-84 years; blood pressure (BP) 125.5 ± 6.4/78.5 ± 2.6 mmHg) and 14 matched sedentary healthy subjects (SH, age 63.8 ± 7.4, range 50-79, years; BP 123.5 ± 5.7/79.9 ± 3.2 mmHg) we evaluated the forearm blood flow (FBF, strain-gauge plethysmography) changes induced by intra-brachial acetylcholine (ACH: 0.15, 0.45, 1.5, 4.5, 15 μg/100 ml/min), an endothelium (END)-dependent agonist, in presence of saline (0.2 ml/100 ml/min), L-NMMA (100 μg/100 ml/min), an antagonist for NO-synthase, vitamin (Vit) C (8 mg/100 ml/min), an antioxidant and finally, during L-NMMA + Vit C infusions. The effect of sodium nitroprusside (SNP, 1, 2, 4 μg/100 ml/min), an END-independent agonist, was also evaluated. SH showed a blunted response to ACH (§p < 0.05) as compared to EA, while the VD to SNP was similar in both groups. In SH L-NMMA did not change ACH-induced VD, and Vit C enhanced (*p < 0.05) the response to ACH and restored (#p < 0.01) the inhibiting effect of L-NMMA. In contrast, in EA L-NMMA blunted (°p < 0.05) the response to ACH, whereas Vit C failed to modify the VD to ACH or the inhibiting effect of L-NMMA (data shown as maximal % increase above baseline): (See Table)In conclusion these data confirm that in SH aging is characterized by END dysfunction caused by a reduced NO availability due to oxidative stress and indicate that this alteration can be prevented by physical training.Am J Hypertens (2000) 13, 241A-242A; doi:S0895-7061(00)00933-X
- Publication
American Journal of Hypertension, 2000, Vol 13, p241A
- ISSN
0895-7061
- Publication type
Article
- DOI
10.1016/S0895-7061(00)00933-X