Voluntary physical exercise-induced vascular effects in spontaneously hypertensive rats

Abstract

Forced training has been shown to have beneficial vascular effects in various animal exercise models. In the present study, we explored possible physiological and molecular effects of voluntary physical exercise on various vascular beds. SHR (spontaneously hypertensive rats) performed voluntary exercise for 5 weeks in a computerized wheel cage facility. Ex vivo myograph studies revealed an increased sensitivity of the ACh (acetylcholine)-mediated vasodilation in resistance arteries of the exercised animals (ED50=15.0+/-3.5 nmol/l) compared with the controls (ED50=37.0+/-8.8 nmol/l; P=0.05). The exercise/control difference was abolished after scavenging reactive oxygen radicals. In conduit arteries, ACh induced a similar vasodilatory response in both groups. The in vivo aortic wall stiffness, assessed by means of Doppler tissue echography, was significantly lower in the exercising animals than in controls. This was demonstrated by significantly increased peak systolic aortic wall velocity (P=0.03) and the velocity time integral (P=0.01) in exercising animals compared with controls. The relative gene expression of eNOS (endothelial nitric oxide synthase) was similar in both groups of animals, whereas Cu/ZnSOD (copper/zinc superoxide dismutase) gene expression was significantly increased (+111%; P=0.0007) in the exercising animal compared with controls. In conclusion, voluntary physical exercise differentially improves vascular function in various vascular beds. Increased vascular compliance and antioxidative capacity may contribute to the atheroprotective effects associated with physical exercise in conduit vessels.

Mechanism behind Augmentation in Baroreflex Sensitivity after Acute Exercise in Spontaneously Hypertensive Rats

“…In the present study, BRS did not change at 30 min or even 60 min after the infusion period in Iso+Phe(low) rats. It is possible that 40-min increases in arterial pressure and HR could not alter arterial distensibility, and thus BRS in SHR, although chronic exercise training seems to increase arterial distensibility (30) and aortic baroreceptor gain sensitivity (31) in SHR. Chandler and DiCarlo (5) have demonstrated that sinoaortic denervation prevents post-exercise reductions in arterial pressure and sympathetic tonus.…”

Effects of aerobic exercise training in animal models of hypertension.

“…(21) Additionally, APT in treadmill was able to increase baroreflex sensitivity in SHR, (22) this being the benefit explained, at least in part, by increasing afferent this reflex arc after APT in SHR rats. (23) Other studies also suggest the reduction of oxidative stress (24), ultrastructural changes in renal morphology, (25,26) reduced expression of angiotensinogen central core, (27) the improvement of vascular compliance (28) and activation of the kallikrein-kinin system (29) could contribute to the improvement of baroreflex and reducing BP after APT in SHR.…”

Regular swimming exercise performed either before or after the induction of renovascular hypertension alleviates oxidative renal injury in rats

“…Accordingly, several potent antioxidants were investigated to be used as antihypertensive agents and were shown to reduce blood pressure by improving baroreflex sensitivity, down-regulating vascular matrix metalloproteinases or scavenging the oxygen radicals that would inactivate vasodilatory action of nitric oxide (NO) (3,4,5). Similar to antioxidants, aerobic exercise training was shown to reduce oxidative stress and inflammation and to increase anti-oxidant defenses by enhancing the resistance against reactive oxygeninduced lipid peroxidation and DNA damage (6,7).Voluntary running exercise in spontaneously hypertensive rats was shown to reduce plasma renin activity and plasma renin concentration (8) and improve microcirculatory profile in different tissues (9,10), making exercise a recommended non-pharmacological treatment modality in hypertension (11,12).…”