Physical Training vs. Perindopril Treatment on Arterial Stiffening of Spontaneously Hypertensive Rats: A Proteomic Analysis and Possible Mechanisms.
Danyelle Siqueira MiottoFrancine DuchatschAline DionizioMarília Afonso Rabelo BuzalafSandra Lia do AmaralPublished in: Biomedicines (2023)
(1) Background: Arterial stiffness is an important predictor of cardiovascular events. Perindopril and physical exercise are important in controlling hypertension and arterial stiffness, but the mechanisms are unclear. (2) Methods: Thirty-two spontaneously hypertensive rats (SHR) were evaluated for eight weeks: SHR C (sedentary); SHR P (sedentary treated with perindopril-3 mg/kg) and SHR T (trained). Pulse wave velocity (PWV) analysis was performed, and the aorta was collected for proteomic analysis. (3) Results: Both treatments determined a similar reduction in PWV (-33% for SHR P and -23% for SHR T ) vs. SHR C , as well as in BP. Among the altered proteins, the proteomic analysis identified an upregulation of the EH domain-containing 2 (EHD2) protein in the SHR P group, required for nitric oxide-dependent vessel relaxation. The SHR T group showed downregulation of collagen-1 (COL1). Accordingly, SHR P showed an increase (+69%) in the e-NOS protein level and SHR T showed a lower COL1 protein level (-46%) compared with SHR C . (4) Conclusions: Both perindopril and aerobic training reduced arterial stiffness in SHR; however, the results suggest that the mechanisms can be distinct. While treatment with perindopril increased EHD2, a protein involved in vessel relaxation, aerobic training decreased COL1 protein level, an important protein of the extracellular matrix (ECM) that normally enhances vessel rigidity.
Keyphrases
- blood pressure
- nitric oxide
- cardiovascular events
- extracellular matrix
- physical activity
- hypertensive patients
- protein protein
- amino acid
- binding protein
- signaling pathway
- poor prognosis
- long non coding rna
- type diabetes
- high intensity
- coronary artery
- small molecule
- hydrogen peroxide
- cardiovascular disease
- single molecule
- replacement therapy
- pulmonary arterial hypertension
- preterm birth
- nitric oxide synthase
- newly diagnosed