Training Attenuated Hypertension in Dexamethasone‐Treated Wistar Rats and SHR Through Different Mechanisms

Abstract

It has been shown that chronic treatment with dexamethasone (DEX) increase blood pressure (BP) in normotensive rats, however, nothing is known about the effects of DEX treatment in spontaneously hypertensive rats (SHR). On the other hand, exercise training (T) has been recommended as a non‐pharmacological treatment for hypertension. Thus, the aim of this study was to investigate the preventive role of T in counteracting DEX‐induced BP increase in normotensive and SHR. Rats were randomly allocated into 8 groups: Wistar sedentary control (WSC), Wistar sedentary treated with DEX (WSD), Wistar trained control (WTC), Wistar trained and treated with DEX (WTD), SHR sedentary control (SHRSC), SHR sedentary treated with DEX (SHRSD), SHR trained control (SHRTC) and SHR trained and treated with DEX (SHRTD). All groups underwent T protocol (treadmill, 60% of physical capacity, 5 days/week, 8 weeks) or were kept sedentary. Then, rats were treated with DEX or saline (0.05 mg/kg per day, s.c., 14 days). Systolic arterial pressure (SAP) was measured by carotid artery catheterization and cardiovascular autonomic modulation to the heart was evaluated by spectral analysis. In addition, tibialis anterior (TA) muscle was collected for morphometric analysis. In Wistar rats, DEX treatment increased SAP (130 ± 5 vs 106 ± 6 mmHg, for SD vs SC, respectively) associated with an increase in low‐frequency spectral power (LF) (45.1 ± 5.9 vs 18.7 ± 4.8 nu, for SD vs SC, respectively) and a decrease in high‐frequency (HF) spectral power (54.8 ± 5.9 vs 81.2 ± 4.8 nu, for SD vs SC, respectively) of pulse interval; also DEX decreased capillary‐to‐fiber ratio (C:F ratio) (0.7 ± 0.02 vs 0.9 ± 0.01, for SD vs SC, respectively) in TA muscle, without affecting wall‐to‐lumen ratio (W/L ratio). Although SHR presented higher SAP (149 ± 7 vs 106 ± 6 mmHg, for SHRSC vs WSC, respectively) and W/L ratio (0.91 ± 0.09 vs 0.58 ± 0.08, for SHRSC vs WSC, respectively) as well as lower values of C:F ratio (0.7 ± 0.04 vs 0.9 ± 0.01, for SHRSC vs WSC, respectively), compared with Wistar rats, DEX treatment did not produce any further alterations in these parameters. On the other hand, T, in Wistar rats, was able to attenuate SAP increase (122 ± 4 vs 130 ± 5 mmHg, for TD vs SD, respectively), LF increase (27.6 ± 6.2 vs 45.1 ± 5.9 nu, for TD vs SD, respectively), HF decrease (72.3 ± 6.2 vs 54.8 ± 5.9 nu, for TD vs SD, respectively) of pulse interval and also C:F ratio decrease (1.0 ± 0.02 vs 0.7 ± 0.02, for TD vs SD, respectively) in TA muscle. In addition, in SHR, T was effective to reduce SAP (121 ± 5 vs 151 ± 8 mmHg, for TD vs SD, respectively), to increase C:F ratio (1.0 ± 0.04 vs 0.7 ± 0.02, for TD vs SD, respectively) and to decrease arterioles W/L ratio (0.58 ± 0.09 vs 0.91 ± 0.08, for TD vs SD, respectively) in TA muscle. In conclusion, these results allow us to suggest that T was able to attenuate DEX‐induced BP increase in Wistar rats, associated with an improvement of cardiovascular autonomic modulation and skeletal muscle microcirculation. In addition, T was able to decrease BP in SHR, mainly through decreases in arterioles W/L ratio and improvements in microcirculation, independent of DEX treatment.Support or Funding InformationSão Paulo Research FoundationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.