Abstract
The imbalance between angiotensin II (Ang II) and angiotensin 1–7 (Ang 1–7) in the brain has been reported to contribute to cardiovascular dysfunction in hypertension. Exercise training (ExT) is beneficial to hypertension and the mechanism is unclear. This study was aimed to determine if ExT improves hypertension via adjusting renin angiotensin system in cardiovascular centers including the rostral ventrolateral medulla (RVLM). Spontaneously hypertensive rats (SHR, 8 weeks old) were subjected to low-intensity ExT or kept sedentary (Sed) for 12 weeks. Blood pressure elevation coupled with increase in age was significantly decreased in SHR received ExT compared with Sed. The results in vivo showed that ExT significantly reduced or increased the cardiovascular responses to central application of sarthran (antagonist of Ang II) or A779 (antagonist of Ang 1–7), respectively. The protein expression of the Ang II acting receptor AT1R and the Ang 1–7 acting receptor Mas in the RVLM was significantly reduced and elevated in SHR following ExT, respectively. Moreover, production of reactive oxygen species in the RVLM was significantly decreased in SHR following ExT. The current data suggest that ExT improves hypertension via improving the balance of Ang II and Ang 1–7 and antioxidative stress at the level of RVLM.
Highlights
Hypertension is characterized by elevated levels of blood pressure (BP) and sympathetic tone, which are associated with the development and prognosis of this disease [1, 2]
Twenty-four-hour urinary excretion of NE level was higher in spontaneously hypertensive rats (SHR)-Sed than in WKY-Sed, whereas it was significantly reduced following Exercise training (ExT) protocol
We confirmed that the concentration of citrate synthase, a marker of ExT efficacy, in soleus muscle was significantly higher in ExT than in Sed rats
Summary
Hypertension is characterized by elevated levels of blood pressure (BP) and sympathetic tone, which are associated with the development and prognosis of this disease [1, 2]. It is well known that the renin-angiotensin system (RAS) has widely cardiovascular regulatory effects and its abnormality participates the generation and development of hypertension [6, 7]. In a classical RAS, angiotensin (Ang) II produced from Ang I by an angiotensin-converting enzyme (ACE) is a strong bioactive substance and its activation contributes to the development of the hypertension [10]. Besides the ACE-Ang II-AT1R axis, recent studies have established a new regulatory axis in the RAS [11]. In this axis, angiotensin (Ang) (1–7) is produced from Ang I or Ang II by the catalytic activity of angiotensin-converting enzyme 2 (ACE2). It has been found that the microinjection of Ang II into the RVLM can cause the higher elevated amplitude of BP, and the expression of AT1R in the spontaneously hypertensive rats (SHR) was higher than in the normotensive rats [13,14,15,16]
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