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2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Antonella De Angelis ◽  
Donato Cappetta ◽  
Marialucia Telesca ◽  
Gabriella Bellocchio ◽  
Konrad Urbanek ◽  
...  

Abstract Aims The majority of elderly patients with heart failure has a preserved ejection fraction (HFpEF) that constitutes a syndrome characterized by frequent hospitalizations and high mortality. Despite the growing social burden of HFpEF, the comprehension of its pathophysiology is incomplete, and treatment remains largely undefined. Ageing itself may contribute independently to deterioration of diastolic function. Methods and results An 18-month-old female Fischer 344 rats were treated with oral administration of either sacubitril/valsartan (60 mg/kg/die, 1:1 ratio) or valsartan alone (30 mg/kg/die) for 12 weeks. Tail-cuff method was used to monitor blood pressure weekly. Echocardiography and left ventricle catheterization were employed to assess systolic and diastolic function, at baseline, and before sacrifice. Cardiac tissue was used for molecular biology and histochemistry assays. Tail-cuff analysis indicated a comparable decrease in blood pressure between treatments. Hypertrophy also showed a significant reduction with both treatments. On the contrary, myocardial function analysis demonstrated that no treatment was efficacy on diastolic dysfunction. The lack of improvement of cardiac function could be attributed to the inability of the treatments to counteract the accumulation of fibrotic tissue in the left ventricle, which, in turn, is attributable to the failure to reduce the inflammatory process and oxidative stress, and to the inability to modulate angiotensin II pathway. Conclusions Our results evidenced that both sacubitril/valsartan or valsartan treatment was able to improve diastolic function and pro-fibrotic remodelling, partly due to a lack of effect on classical and non-classical pathways of angiotensin II.


Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 424
Author(s):  
Perla Y. Gutiérrez-Arzapalo ◽  
Pilar Rodríguez-Rodríguez ◽  
David Ramiro-Cortijo ◽  
Marta Gil-Ortega ◽  
Beatriz Somoza ◽  
...  

Fetal undernutrition programs hypertension and cardiovascular diseases, and resistance artery remodeling may be a contributing factor. We aimed to assess if fetal undernutrition induces resistance artery remodeling and the relationship with hypertension. Sprague–Dawley dams were fed ad libitum (Control) or with 50% of control intake between days 11 and 21 of gestation (maternal undernutrition, MUN). In six-month-old male and female offspring we assessed blood pressure (anesthetized and tail-cuff); mesenteric resistance artery (MRA) structure and mechanics (pressure myography), cellular and internal elastic lamina (IEL) organization (confocal microscopy) and plasma MMP-2 and MMP-9 activity (zymography). Systolic blood pressure (SBP, tail-cuff) and plasma MMP activity were assessed in 18-month-old rats. At the age of six months MUN males exhibited significantly higher blood pressure (anesthetized or tail-cuff) and plasma MMP-9 activity, while MUN females did not exhibit significant differences, compared to sex-matched controls. MRA from 6-month-old MUN males and females showed a smaller diameter, reduced adventitial, smooth muscle cell density and IEL fenestra area, and a leftward shift of stress-strain curves. At the age of eighteen months SBP and MMP-9 activity were higher in both MUN males and females, compared to sex-matched controls. These data suggest that fetal undernutrition induces MRA inward eutrophic remodeling and stiffness in both sexes, independent of blood pressure level. Resistance artery structural and mechanical alterations can participate in the development of hypertension in aged females and may contribute to adverse cardiovascular events associated with low birth weight in both sexes.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S93-S93
Author(s):  
Mafalda Cacciottolo ◽  
Todd E Morgan ◽  
Caleb E Finch

Abstract Cerebral microbleeds (MBs) contribute to pre-clinical cognitive decline and are an additional clinical burden in Alzheimer Disease (AD). Hypertension is associated with MBs, with nearly 2-fold higher likelihood for MBs per SD increment in blood pressure (BP). We investigated the possible role of age-related hypertension in the EFAD mouse model (transgenic for carrying familial AD mutations and targeted replacement of human APO-E3 or -E4). MBs were detected by Prussian Blue histochemistry. We extended prior findings with observations that MBs arise early in life, by 2 months, and confirmed female excess for ApoE3 and-E4 carriers. Wildtype C57BL/6J mice also accumulated MBs, and a 10-fold lower level and more slowly up to 21mo of age. BP was measured by the tail-cuff method. All mice had BP in the normotensive range, <150 mm Hg, systolic. Longitudinal measurements of blood pressure at ages 2, 4, and 6 months showed few age changes, except for E3FAD females at 6 months (systolic, +20%, p<0.05; diastolic, +33%, p<0.05). A possible decrease in blood pressure was observed in EFAD mice (-33%, p<0.01) compared to C57BL/6J mice. A not statistical trend of increase was observed in older C57BL/6J mice up to 18 mo of age, consistent with previous reports. Older ages are required for complete negation of role of hypertension in the MB model. Ongoing studies will examine mice older than 6 months for potential relations of blood pressure and MB, and in relation to brain amyloid deposits which surrounded MBs in our prior study.


2019 ◽  
Vol 96 (1) ◽  
pp. 34-36 ◽  
Author(s):  
James Matthew Luther ◽  
Agnes B. Fogo
Keyword(s):  

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Rafaela Feresin ◽  
Rami Najjar ◽  
Christy Simecka ◽  
Shengyu Mu

Abstract Objectives To examine whether diet supplementation with blackberry or raspberry attenuate angiotensin (Ang) II-induced increase in blood pressure (BP) and decrease oxidative stress in the kidneys of mice. Methods Twelve-week male C57BL/6 J mice were fed AIN-93 M diets alone (control and Ang II groups) or supplemented with 10% w/w freeze-dried blackberry (BL + Ang II) or raspberry (RB + Ang II) powder for eight weeks. At week 4, mice were implanted with subcutaneous osmotic minipumps that delivered 0.9% saline (Control) or Ang II (1 µg/kg body weight/day) for another four weeks. BP was measured weekly by tail-cuff plethysmography and validated by direct measurement at endpoint using a BP catheter. Kidney expression of pro-oxidant enzymes such as NADPH oxidases (Nox) and antioxidant enzymes such as superoxide dismutates (SOD) were also measured. Results were analyzed using ANOVA followed by Tukey-Kramer post-hoc test. Results As expected, Ang II significantly increased systolic BP (SBP; 185 ± 4, n = 6, vs 132 ± 2 mmHg, n = 5, P < 0.001) and diastolic BP (124 ± 4, n = 6, vs 96 ± 2 mmHg, n = 4, P < 0.001) compared to control. Supplementation with BL and RB significantly attenuated this increase in SBP (143 ± 7 mmHg, n = 5, P < 0.0001 and 137 ± 4 mmHg, n = 5, P < 0.0001, respectively) and DBP (100 ± 6 mmHg, n = 5, P < 0.003 and 90 ± 3 mmHg, n = 5, P < 0.0001, respectively). Regarding the expression of NADPH oxidases in the kidney, Nox2 was significantly decreased by supplementation with BL (0.68 ± 0.07-fold, n = 5, P = 0.0005) and RB (0.70 ± 0.03-fold, n = 5, P = 0.0008) compared to Ang II (1.15 ± 0.12-fold, n = 5). Nox1 expression was up-regulated by Ang II compared to control (2.03 ± 0.16 vs 1.00 ± 0.00-fold, n = 5, P = 0.0001), but this was not prevented by supplementation with either berry. Nox4 expression was not affected by any of the treatments. Lastly, Ang II did not change the expression of SOD1 and SOD2 in the kidney, however, supplementation with RB significantly increased SOD1 (P = 0.02) and SOD2 (P = 0.005) expression compared to the other groups. Conclusions Our findings indicate that supplementation with BL and RB decrease BP in mice which may be related to a decrease in oxidative stress in the kidney. Studies are underway to further elucidate the mechanism by which BL and RB exert their antihypertensive effects. Funding Sources Arkansas Biosciences Institute and Lewis Foundation Grant Program.


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