Acute resistance exercise reduces blood pressure and vascular reactivity, and increases endothelium-dependent relaxation in spontaneously hypertensive rats

Abstract

The aim of the present study was to assess the effects of acute dynamic resistance exercise on resting blood pressure (BP) and on endothelial function of vascular bed of spontaneously hypertensive rats. Hemodynamic measurements were performed before and after acute dynamic resistance exercise in conscious animals. After exercise, the tail artery was cannulated for mean perfusion pressure with constant flow measurement and for performing concentration-response curves to acetylcholine (ACh) and sodium nitroprusside (SNP) and dose-response curves to phenylephrine (PHE). PHE protocol was also repeated with damaged endothelium and after L-NAME and indomethacin perfusion on the tail. The maximal response (E(max)) and sensitivity (pD(2)) were evaluated to these drugs. Exercise reduced resting systolic and diastolic BP (Delta -79 +/- 1.8; -23 +/- 2.3 mmHg, respectively; P < 0.05). ACh-induced relaxation increased in the exercise group (pD(2) = 9.8 +/- 0.06, P < 0.05) when compared with control rats (pD(2) = 8.7 +/- 0.1). The E(max) to PHE with intact endothelium decreased following exercise condition (439 +/- 18 mmHg, P < 0.05) when compared with control rats (276 +/- 22 mmHg). This response was abolished after L-NAME and indomethacin administration. After damage of the endothelium, PHE responses were not significantly different between the groups; however, E(max) and pD(2) increased when compared with responses obtained with intact endothelium. The results demonstrated that acute dynamic resistance exercise decreased resting BP and reactivity to PHE and increased endothelium-dependent relaxation. Nitric oxide and vasodilators prostanoids appear to be involved in post-exercise endothelial and pressor responses.

NanoUPLC/MSE proteomic analysis reveals modulation on left ventricle proteome from hypertensive rats after exercise training

“…Moreover, the SBP of untrained rats presented a significant elevation (SHR-C; Δ 13.5 mmHg − 1 ) at the end of the experimental period (Table 1). This response is in accordance with several studies, where different exercise regimens and intensities are shown to reduce SBP and improve cardiovascular fitness [48,49,[56][57][58], also contributing to interrupt pathological hypertrophy in SHR rats [59]. Besides LVH, other pathologic parameters such as collagen and wallto-lumen ratio were also shown to be reduced in hypertensive rats after treadmill training [60].…”

Inflammatory and Biochemical Biomarkers in Response to High Intensity Resistance Training in Trained and Untrained Men

“…After training, blood pressure reduced within minutes after training and remained at low levels of baseline for hours. This phenomenon is called post-exercise hypotension (PEH) (31). Previously, it has been shown that PEH is occurred either by continuous dynamic training such as running and cycling or intermittent training such as resistance exercise (32).…”

Impact of exercise training on redox signaling in cardiovascular diseases

“…These improvements are linked to increased vascular NO Å bioavailability and reduced oxidant stress. Of interest, a single bout of either aerobic or resistance exercise increases endothelial-dependent relaxation through NO Å pathways (Faria Tde et al, 2010;Yang et al, 2010). Moreover, improved NOS activity and diminished ROS production have been associated with better vascular function in hypertensive rats submitted to either moderate-or high-intensity aerobic exercise training (Blanco-Rivero et al, 2013;Kimura et al, 2010;Roque et al, 2013a,b;Yang et al, 2011).…”