Physical Training vs. Perindopril Treatment on Arterial Stiffening of Spontaneously Hypertensive Rats: A Proteomic Analysis and Possible Mechanisms

Author:

Miotto Danyelle Siqueira1,Duchatsch Francine1,Dionizio Aline2,Buzalaf Marília Afonso Rabelo2ORCID,Amaral Sandra Lia13ORCID

Affiliation:

1. Joint Graduate Program in Physiological Sciences (PIPGCF), Federal University of Sao Carlos and São Paulo State University, UFSCar/UNESP, São Carlos 14801-903, Brazil

2. Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo—USP, Bauru 17012-901, Brazil

3. Department of Physical Education, School of Sciences, São Paulo State University—UNESP, Bauru 17033-360, Brazil

Abstract

(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: SHRC (sedentary); SHRP (sedentary treated with perindopril—3 mg/kg) and SHRT (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 SHRP and −23% for SHRT) vs. SHRC, 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 SHRP group, required for nitric oxide-dependent vessel relaxation. The SHRT group showed downregulation of collagen-1 (COL1). Accordingly, SHRP showed an increase (+69%) in the e-NOS protein level and SHRT showed a lower COL1 protein level (−46%) compared with SHRC. (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.

Funder

São Paulo Research Foundation

the National Council for Scientific and Technological Development

Coordination for the Improvement of Higher Education Personnel—Brazil

Coordination for the Improvement of Higher Education Personnel

Publisher

MDPI AG

Subject

General Biochemistry, Genetics and Molecular Biology,Medicine (miscellaneous)

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