Low-Intensity exercise attenuates hypertensive vascular injury and is associated with improved endothelial-related signaling and modulated vascular inflammatory status in spontaneously hypertensive rats

Q: What are the key findings of this study?

Low-intensity treadmill exercise for 12 weeks reduced blood pressure by approximately 15-20 mmHg and attenuated vascular remodeling compared with sedentary spontaneously hypertensive rats.

Q: What is the clinical evidence from this study?

Population: Hypertension (n=50). Intervention: Low-intensity treadmill exercise (alone or combined with Valsartan) vs. Sedentary spontaneously hypertensive rats (vehicle gavage) and normotensive WKY controls. Primary outcome: Invasive systolic blood pressure at week 12 (MD -15 to -20 mmHg, p=<0.05).

Q: What does this research mean for the field?

Low-intensity treadmill exercise reduces blood pressure by 15–20 mmHg and attenuates hypertensive vascular remodeling in spontaneously hypertensive rats. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To determine whether low-intensity treadmill exercise attenuates vascular injury in spontaneously hypertensive rats and explore the associated molecular and multi-omics mechanisms.

Chunrui Hu; Qiuting Yu; Qiong Wu; Xiang Zhang; Peng Wang; Tianyi Chen; Zilin Ma; Xinlin Chen; Wei Chen

doi:10.1186/s13102-026-02214-6

November 5, 2026BMC Sports Science Medicine and RehabilitationOpen Access

Low-Intensity exercise attenuates hypertensive vascular injury and is associated with improved endothelial-related signaling and modulated vascular inflammatory status in spontaneously hypertensive rats

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Key result

Low-intensity treadmill exercise lowers systolic blood pressure ~18 mmHg and attenuates vascular remodeling in hypertensive rats.

MD -15 to -20 mmHg
P<0.05
n=50

Why the study?

Essential hypertension is characterized by persistent vascular dysfunction, endothelial impairment, and chronic low-grade inflammation. Whether low-intensity treadmill exercise attenuates vascular injury in spontaneously hypertensive rats and the associated molecular mechanisms required investigation.

Does low-intensity treadmill exercise (alone or combined with valsartan) reduce systolic blood pressure and attenuate hypertensive vascular injury in spontaneously hypertensive rats?

Key Points

To determine whether low-intensity treadmill exercise attenuates vascular injury in spontaneously hypertensive rats and explore the associated molecular and multi-omics mechanisms.
Male spontaneously hypertensive rats were randomly assigned to sedentary, low-intensity exercise, positive-control drug, or combined intervention groups, with normotensive Wistar-Kyoto rats as controls (n = 10 per group).
Exercising rats performed a 12-week treadmill protocol at 20 m/min for 60 min/day, 5 days/week.
Blood pressure, abdominal aortic hemodynamics, serum vasoactive and lipid markers, vascular histology, macrophage markers, and PI3K/Akt/eNOS signaling were evaluated.
Low-intensity exercise significantly reduced systolic, diastolic, and mean arterial pressure starting at week 4, producing a final reduction of approximately 15–20 mmHg compared with sedentary hypertensive rats.
Exercise attenuated abdominal aortic wall thickening and lumen narrowing, decreased serum Ang II and ET-1, increased circulating NO-related analytes, and reduced TG, TC, and LDL-C levels.
Aortic tissue showed increased p-PI3K/PI3K, p-Akt/Akt, and p-eNOS/eNOS ratios, decreased GPR68 expression, and a shift from CD80-positive M1 to CD206-positive M2 macrophages.

Structured PICO

Does low-intensity treadmill exercise (alone or combined with valsartan) reduce systolic blood pressure and attenuate hypertensive vascular injury in spontaneously hypertensive rats?

P

Population

50 male spontaneously hypertensive and normotensive Wistar-Kyoto rats (aged 6-8 weeks, 200-300 g) randomized into five groups and followed for 12 weeks.

I

Intervention

Low-intensity motorized treadmill running at 20 m/min (5% incline) for 60 min/day, 5 days/week, for 12 consecutive weeks (plus equivalent vehicle gavage), either alone or combined with daily intragastric administration of valsartan 10 mg/kg/day for 12 weeks.

C

Comparator

Sedentary spontaneously hypertensive rats (SHR group) receiving equivalent vehicle gavage, positive-control drug group receiving intragastric valsartan 10 mg/kg/day for 12 weeks, and normotensive control group (WKY rats) (n=10 per group).

O

Outcome

Invasive systolic blood pressure (SBP) at week 12.surrogate

Main Result

Effect estimate: MD -15 to -20 mmHg

p-value: p=<0.05

Limitations

Preclinical animal model (male spontaneously hypertensive rats only)
Tail-cuff blood pressure measurements were performed by an operator aware of group allocation
Cage was not included as a statistical factor despite group housing
Abdominal aortas were fixed without controlled intraluminal pressure for histology
Causal mediation of the PI3K/Akt/eNOS pathway was not tested by pathway inhibition
Multi-omics contrasts compared combined intervention (exercise plus valsartan) versus SHR and could not isolate an exercise-specific systems-level effect
Several serum metabolite annotations likely reflect exogenous or dietary exposure rather than endogenous metabolism
Sample size was determined a priori for the primary blood-pressure endpoint rather than for multi-omics layers (RNA-seq performed with n=3 biological replicates per group)
Animals were group-housed (5 per cage) and cage was not included as a statistical factor
The same operator performed all tail-cuff measurements with knowledge of group allocation
Abdominal aortas were fixed in 4% paraformaldehyde without controlled intraluminal pressure
Pathway changes (PI3K/Akt/eNOS and GPR68) are associated with the observed vascular phenotype, but mediation was not tested by pathway inhibition
Multi-omics contrasts (combined intervention vs. SHR) characterize the molecular profile of the combined exercise-plus-drug intervention and do not isolate an exercise-specific systems-level effect

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Implication

In spontaneously hypertensive rats, 12 weeks of low-intensity treadmill exercise lowers blood pressure by 15–20 mmHg and attenuates vascular remodeling, accompanied by enhanced aortic PI3K/Akt/eNOS signaling and an anti-inflammatory M2 macrophage shift.

Abstract

Essential hypertension is characterized by persistent vascular dysfunction, endothelial impairment, and chronic low-grade inflammation. The present study investigated whether low-intensity treadmill exercise attenuates vascular injury in spontaneously hypertensive rats (SHRs) and explored associated molecular mechanisms using physiological, molecular, and multi-omics approaches. Male SHRs were randomly assigned to sedentary SHR, low-intensity exercise, positive-control drug, and combined intervention groups, with age-matched Wistar-Kyoto (WKY) rats serving as normotensive controls ( n = 10 per group). Rats in the exercise groups underwent a 12-week treadmill protocol at 20 m/min for 60 min/day, 5 days/week. Low-intensity exercise progressively reduced systolic, diastolic, and mean arterial pressure, with significant antihypertensive effects emerging after 4 weeks and a final reduction of approximately 15–20 mmHg compared with sedentary SHRs. Exercise also improved abdominal aortic hemodynamic indices, attenuated vascular wall thickening, improved lipid-related markers, decreased angiotensin II and endothelin-1, and increased the circulating NO-related analyte measured by ELISA. In aortic tissue, exercise was associated with activation of PI3K/Akt/eNOS signaling, reduced GPR68 expression. Integrated transcriptomic, proteomic, and serum metabolomic analyses (contrasting SHR vs. WKY and combined intervention vs. SHR) identified convergent changes in inflammatory signaling, extracellular matrix organization, nitric oxide–cGMP–PKG signaling, lipid metabolism, and arginine-related metabolism. Collectively, these findings indicate that low-intensity treadmill exercise attenuates hypertensive vascular injury and that its protective profile is associated with coordinated endothelial-related, immuno-inflammatory, and metabolic alterations.

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Cite This Study

Hu et al. (2026) studied Hypertension (n=50). Low-intensity treadmill exercise (alone or combined with Valsartan) vs. Sedentary spontaneously hypertensive rats (vehicle gavage) and normotensive WKY controls was evaluated on Invasive systolic blood pressure at week 12 (MD -15 to -20 mmHg, p=<0.05). Low-intensity treadmill exercise for 12 weeks reduced blood pressure by approximately 15-20 mmHg and attenuated vascular remodeling compared with sedentary spontaneously hypertensive rats.

synapsesocial.com/papers/6aee6bc771a7594806220b98 https://doi.org/10.1186/s13102-026-02214-6

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Low-Intensity exercise attenuates hypertensive vascular injury and is associated with improved endothelial-related signaling and modulated vascular inflammatory status in spontaneously hypertensive rats

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Low-Intensity exercise attenuates hypertensive vascular injury and is associated with improved endothelial-related signaling and modulated vascular inflammatory status in spontaneously hypertensive rats

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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