Effects of High-intensity Interval Exercise on Blood Lipids and Renin-angiotensin System (RAS)-related Factors in Ovariectomized Rats

Author(s):  
Eun-Mi Lim ◽  
Ze-One Kim ◽  
Jin-Hwan Yoon
2016 ◽  
Vol 311 (5) ◽  
pp. R898-R905 ◽  
Author(s):  
Shoko Tazumi ◽  
Naoko Yokota ◽  
Mizuho Kawakami ◽  
Sayo Omoto ◽  
Akira Takamata ◽  
...  

The purpose of this study was to determine whether chronic estrogen replacement in ovariectomized rats inhibits the pressor response to psychological stress by attenuating the activation of the renin-angiotensin system. Female Wistar rats aged 9 wk were ovariectomized. After 4 wk, the rats were randomly assigned to be implanted subcutaneously with pellets containing either 17β-estradiol (E2) or placebo (Pla). After 4 wk of treatment, the rats underwent cage-switch stress and, in a separate experiment, a subset received an infusion of angiotensin II. The cage-switch stress rapidly elevated blood pressure (BP) and heart rate (HR) as measured by radiotelemetry in both groups. However, the BP and HR responses to the stress were significantly attenuated in the E2 group compared with the Pla group. An angiotensin II type 1 receptor blocker, losartan, given in drinking water, abolished the difference in the pressor response to stress between the two groups. Moreover, the stress-induced elevation in plasma renin activity and angiotensin II concentration was significant in the Pla group, but not in the E2 group. In addition, the expression of renin mRNA in the kidney was lower in the E2 group relative to the Pla group. Finally, we found that intravenous angiotensin II infusion increased BP and decreased HR to a similar degree in both groups. These results suggest that the inhibitory effects of estrogen on psychological stress-induced activation of the renin-angiotensin system could be at least partially responsible for the suppression of the pressor responses to psychological stress seen in estrogen-replaced ovariectomized rats.


Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6945
Author(s):  
George El-Arif ◽  
Antonella Farhat ◽  
Shaymaa Khazaal ◽  
Cédric Annweiler ◽  
Hervé Kovacic ◽  
...  

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), was first identified in Eastern Asia (Wuhan, China) in December 2019. The virus then spread to Europe and across all continents where it has led to higher mortality and morbidity, and was declared as a pandemic by the World Health Organization (WHO) in March 2020. Recently, different vaccines have been produced and seem to be more or less effective in protecting from COVID-19. The renin–angiotensin system (RAS), an essential enzymatic cascade involved in maintaining blood pressure and electrolyte balance, is involved in the pathogenicity of COVID-19, since the angiotensin-converting enzyme II (ACE2) acts as the cellular receptor for SARS-CoV-2 in many human tissues and organs. In fact, the viral entrance promotes a downregulation of ACE2 followed by RAS balance dysregulation and an overactivation of the angiotensin II (Ang II)–angiotensin II type I receptor (AT1R) axis, which is characterized by a strong vasoconstriction and the induction of the profibrotic, proapoptotic and proinflammatory signalizations in the lungs and other organs. This mechanism features a massive cytokine storm, hypercoagulation, an acute respiratory distress syndrome (ARDS) and subsequent multiple organ damage. While all individuals are vulnerable to SARS-CoV-2, the disease outcome and severity differ among people and countries and depend on a dual interaction between the virus and the affected host. Many studies have already pointed out the importance of host genetic polymorphisms (especially in the RAS) as well as other related factors such age, gender, lifestyle and habits and underlying pathologies or comorbidities (diabetes and cardiovascular diseases) that could render individuals at higher risk of infection and pathogenicity. In this review, we explore the correlation between all these risk factors as well as how and why they could account for severe post-COVID-19 complications.


Life Sciences ◽  
2017 ◽  
Vol 189 ◽  
pp. 8-17 ◽  
Author(s):  
Guilherme de Oliveira Sá ◽  
Vívian dos Santos Neves ◽  
Shyrlei R. de Oliveira Fraga ◽  
Vanessa Souza-Mello ◽  
Sandra Barbosa-da-Silva

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Yu Nagatomo ◽  
Shoko Tazumi ◽  
Risa Itoh ◽  
Misa Yoshimoto ◽  
Akira Takamata ◽  
...  

2019 ◽  
Vol 42 (3) ◽  
pp. 233-238
Author(s):  
Jeeser Alves Almeida ◽  
Daisy Motta-Santos ◽  
Bernardo Assis Petriz ◽  
Clarissa Pedrosa da Costa Gomes ◽  
Murilo Esteves Nogueira ◽  
...  

Life Sciences ◽  
2013 ◽  
Vol 93 (22) ◽  
pp. 820-829 ◽  
Author(s):  
Antonio Celso S. Ramos-Filho ◽  
Juliana A. Faria ◽  
Fabiano B. Calmasini ◽  
Simone A. Teixeira ◽  
Fabíola Z. Mónica ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document