Abstract

The present study sought to determine cardiovascular effects of aerobic training associated with diminazene aceturate (DIZE), an activator of the angiotensin converting enzyme 2, in spontaneously hypertensive rats (SHRs). Male SHRs (280–350 g) were either subjected to exercise training or not (sedentary group). The trained group was subjected to 8 weeks of aerobic training on a treadmill (five times a week, lasting 60 min at an intensity of 50–60% of maximum aerobic speed). In the last 15 days of the experimental protocol, these groups were redistributed into four groups: i) sedentary SHRs with daily treatment of 1 mg/kg DIZE (S+D1); ii) trained SHRs with daily treatment of 1 mg/kg DIZE (T+D1); iii) sedentary SHRs with daily treatment of vehicle (S+V); and iv) trained SHRs with daily treatment of vehicle (T+V). After treatment, SHRs were anesthetized and subjected to artery and femoral vein cannulation prior to the implantation of ECG electrode. After 24 h, mean arterial pressure (MAP) and heart rate (HR) were recorded; the baroreflex sensitivity and the effect of double autonomic blockade (DAB) were evaluated in non-anesthetized SHRs. DIZE treatment improved baroreflex sensitivity in the T+D1 group as compared with the T+V and S+D1 groups. The intrinsic heart rate (IHR) and MAP were reduced in T+D1 group as compared with T+V and S+D1 groups. Hence, we conclude that the association of exercise training with DIZE treatment improved baroreflex function and cardiovascular regulation.

Highlights

  • Aerobic exercise has been reported as a nonpharmacological antihypertensive therapy (1–5)

  • Running speed performance The speed of the aerobic training increased in both trained groups (T+V: 26.3±0.3 to 41.2±0.6 and T+D1: 26.7±0.4 to 42.0±0.8 m/min, Po0.05)

  • Exercise training promoted a decrease in SBP, DBP, and MAP (T+V: 187.2±4.4, 121.1±4.7, 143.2±4.3 mmHg, respectively, Po0.05) compared with sedentary SHRs (S+V: 212.5±3.6, 135.3±5.1, 161.0±4.3 mmHg, respectively; Figure 1)

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Summary

Introduction

Aerobic exercise has been reported as a nonpharmacological antihypertensive therapy (1–5). Some studies have shown that aerobic exercise could promote a decrease in sympathetic activity (5), a physiological hypertrophy of the left ventricle (1) and improve the vascular reactivity (1,2). Some studies have suggested the existence of a relationship between exercise and renin-angiotensin system (RAS), more studies are needed to verify the role of RAS (4,7). There is growing evidence in support of the relationship between high BP and cardiovascular complications (2). High BP and decreased baroreflex sensitivity are indicators of hypertension (5,8,9). A decrease in baroreflex sensitivity has been reported in patients with post-myocardial infarction (10) and renal failure (11). The integrity of baroreflex sensitivity is important in the preservation and maintenance of cardiovascular homeostasis

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