CHRONIC EXERCISE ENHANCES ENDOTHELIUM-MEDIATED DILATION IN SPONTANEOUSLY HYPERTENSIVE RATS

This study investigated the effect of physical training on endothelial function in spontaneously hypertensive rats (SHR). After 3 months, in conscious trained- and untrained-SHR body weight, systolic blood pressure and heart rate were 220+/-5 g vs. 271+/-9 g, 172+/-7 mmHg vs. 210+/-8 mmHg and 314+/-10 vs. 348+/-12 beats/min, respectively. In vitro, the dose-response curves of norepinephrine in isolated intact aortic and mesenteric rings from the exercise trained-SHR were significantly lower than those from the untrained-SHR. With denuded preparations, norepinephrine concentration-response curves were shifted to the left both in the trained- and untrained-SHR. This shift in the trained-SHR exceeded that in the untrained-SHR. The vasodilator response to acetylcholine in the trained-SHR was significantly greater than that in the untrained-SI-IX, Either N-omega-nitro-L-arginine (100 mu mol/l) or methylene blue (10 mu mol/l) inhibited acetylcholine-induced vasodilator effect in aorta of trained- and untrained-SHR, but not in mesenteric artery of trained-SHR. Tetraethylammonium (10 mmol/l) inhibited significantly the N-omega-nitro-L-arginine and methylene blue-resistant relaxation in mesenteric artery of trained-SHR, but not by indomethacin (10 mu mol/l). Collectively, these data demonstrate that chronic exercise increases EDRF/EDHF production (presumably by increasing endothelial shear stress), and may contribute to the enhanced effects of post-exercise hypotension.(1)