Abstract
Chronic hypertension causes structural changes in the resistance vasculature through the process of remodeling. Middle cerebral artery (MCA) remodeling increases the risk for ischemic stroke. We have previously shown that the mineralocorticoid receptor (MR) is involved in MCA remodeling. Therefore, we hypothesized that MR antagonism with canrenoic acid (CANR) would attenuate the process. Six‐week old male stroke‐prone spontaneously hypertensive rats (SHRSP) were treated with CANR (20mg/kg/day, n=7) in the drinking water for six weeks. Untreated SHRSP were used as controls (n=12). MCA and mesenteric resistant artery (MRA) passive structure was analyzed by pressure myography. Data are shown as mean ± SEM, CANR vs control respectively. In the MCA, at 80mmHg, CANR treatment increased lumen diameter (277±6 vs 240±5μm, p<0.05) and decreased wall thickness (17.1±1.1 vs 25.6±1.2μm, p<0.05) and wall‐to‐lumen ratio (0.06±0.01 vs 0.11±0.01, p<0.05), without changing vessel stiffness (β‐coefficient: 10.4±1.4 vs 8.16±1.6, p<0.05). In the MRA, at 90 mmHg, CANR treatment reduced wall thickness (17.0±0.7 vs 27±1.7μm, p<0.05) and wall‐to‐lumen ratio (0.16±0.01 vs 0.10±0.01, p<0.05), without changing lumen diameter (274±8 vs 265±9μm) or vessel stiffness (β‐coefficient: 5.5±0.7 vs 5.5±0.5). These data suggest that MR antagonism attenuates cerebral and peripheral remodeling by different mechanisms.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
