scholarly journals Renin-angiotensin System (RAS)-mediated Antiobesity and Antihypertensive Effects of Korean Traditional Soybean Paste (Doenjang) in Rat Model of Diet-induced Obesity (P08-097-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Hayoung Woo ◽  
Jung Eun Park ◽  
Youn-soo Cha
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
High Fat Diet ◽  
Health Benefits ◽  
Renin Angiotensin System ◽  
Serum Chemistry ◽  
Table Salt ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin

Abstract Objectives Hypertension is becoming more prevalent and one of the main cause is found in the increase of excessive dietary sodium intake. It is also risk factors for cardiovascular and kidney disease. Korean Traditional Fermented Food, doenjang, is made with high salt, so many of them are thinking that there is a lot of relation to hypertension despite reporting many health benefits. Our previous studies reported that doenjang have been associated effect of anti-obesity in human and animal study. Therefore, we expected that doenjang may have different effects on blood pressure and lipid metabolism compared to same concentrations of salt. Methods In this study, Sprague-Dawley rats divided into four groups, normal diet (ND), high fat diet (HD), high fat diet with 8% table salt (HDS), high fat diet with Doenjang contains 8% table salt (HDJ) for 13 weeks. The systolic blood pressure (SBP), serum chemistry, Na+ and K+ concentrations, liver and renal gene expressions were measured. Results Doenjang decreased systolic blood pressure (SBP), body weight and hepatic lipids. Serum chemistry, leptin and aldosterone levels were increased in HD and HDS groups while decreased in HDJ group. Results from analysing feces and urine, Na+, Ca+ and K+concentrations were changed by Doenjang. Furthermore, fatty acid synthesis-related genes expression was decreased in liver and downregulated the renin, AT1 receptor and ACE in renal cortex of doenjang treatment group. Conclusions These results suggest that doenjang may have anti-obesity and anti-hypertension through regulation of the renin angiotensin system. We believed that it is an important result of demonstrating that doenjang has health benefits regardless of salt content. Funding Sources This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MEST) (No. 2018R1A2B6006477).

scholarly journals Losartan prevents the elevation of blood pressure in adipose-PRR deficient female mice while elevated circulating sPRR activates the renin-angiotensin system

2019 ◽  
Vol 316 (3) ◽  
pp. H506-H515 ◽  
Author(s):  
Eva Gatineau ◽  
Dianne M. Cohn ◽  
Marko Poglitsch ◽  
Analia S. Loria ◽  
Ming Gong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Renin Angiotensin System ◽  
Soluble Form ◽  
Ang Ii ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Female Mice ◽  
Prorenin Receptor

Deletion of the prorenin receptor (PRR) in adipose tissue elevates systolic blood pressure (SBP) and the circulating soluble form of PRR (sPRR) in male mice fed a high-fat (HF) diet. However, sex differences in the contribution of adipose-PRR and sPRR to the regulation of the renin-angiotensin system (RAS) in key organs for blood pressure control are undefined. Therefore, we assessed blood pressure and the systemic and intrarenal RAS status in adipose-PRR knockout (KO) female mice. Blockade of RAS with losartan blunted SBP elevation in HF diet-fed adipose-PRR KO mice. ANG II levels were significantly increased in the renal cortex of HF diet-fed adipose-PRR KO female mice, but not systemically. HF diet-fed adipose-PRR KO mice exhibited higher vasopressin levels, water retention, and lower urine output than wild-type (WT) mice. The results also showed that deletion of adipose-PRR increased circulating sPRR and total hepatic sPRR contents, suggesting the liver as a major source of elevated plasma sPRR in adipose-PRR KO mice. To mimic the elevation of circulating sPRR and define the direct contribution of systemic sPRR to the regulation of the RAS and vasopressin, C57BL/6 female mice fed a standard diet were infused with recombinant sPRR. sPRR infusion increased plasma renin levels, renal and hepatic angiotensinogen expression, and vasopressin. Together, these results demonstrate that the deletion of adipose-PRR induced an elevation of SBP likely mediated by an intrarenal ANG II-dependent mechanism and that sPRR participates in RAS regulation and body fluid homeostasis via its capacity to activate the RAS and increase vasopressin levels. NEW & NOTEWORTHY The elevation of systolic blood pressure appears to be primarily mediated by cortical ANG II in high-fat diet-fed adipose-prorenin receptor knockout female mice. In addition, our data support a role for soluble prorenin receptor in renin-angiotensin system activation and vasopressin regulation.

Abstract P316: Angiotensin-(1-7) Contributes to the Insulin-sensitizing Effects of Renin-angiotensin System Blockade in High Fat Fed Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Amy C Arnold
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Whole Body ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin

Angiotensin-converting enzyme (ACE) inhibitors reduce body weight, lower blood pressure, and improve glucose homeostasis in animal models of the cardiometabolic syndrome. These effects are generally attributed to a reduction in angiotensin (Ang) II formation; however, these therapies also increase circulating levels of Ang-(1-7), a peptide with direct anti-hypertensive and insulin-sensitizing effects. In this study, it was hypothesized that endogenous Ang-(1-7) generation contributes to the beneficial cardiometabolic effects of ACE inhibition. To test this hypothesis, diet-induced obesity was produced in adult male C57BL/6J mice by placing them on a 60% high fat diet for 11 weeks. The Ang-(1-7) mas receptor antagonist A779 (400 ng/kg/min) or saline was given after 8 weeks of the high fat diet by subcutaneous osmotic mini-pumps. Immediately following mini-pump implantation, mice received water containing the ACE inhibitor captopril (50 mg/L) or plain tap water. Hyperinsulinemic (4 mU/kg/min) euglycemic clamps were performed in conscious, unrestrained vehicle (n=6), captopril (n=6), or captopril plus A779 (n=13) mice at the end of the 3-week treatment period. Blood pressure was measured via an indwelling carotid artery catheter connected to a transducer on the morning of the clamp. Captopril reduced body weight (28±2 vs. 41±2 g vehicle; p=0.001), lowered blood pressure (systolic: 109±6 vs.144±7 mmHg vehicle; p=0.003), and improved whole-body insulin sensitivity (steady-state glucose infusion rate: 31±4 vs. 16±2 mg/kg/min; p=0.008) in high-fat fed mice. Mas receptor antagonism with A779 attenuated the improvement in insulin sensitivity produced by captopril in high fat fed mice (23±2 mg/kg/min; p=0.042). There was no effect of A779 on the weight loss (32±2 g) or blood pressure lowering effects (111±7 mmHg) of captopril. These findings suggest that the improvement in insulin sensitivity produced by ACE inhibition is at least partly mediated by Ang-(1-7) pathways, and provide new insight into potential mechanisms involved in renin-angiotensin system blockade.

scholarly journals EFFECT OF SEQUENTIAL NEPHRON BLOCKING IN COMPARISON WITH THE DOUBLE BLOCKADE OF THE RENIN- ANGIOTENSIN SYSTEM + BISOPROLOL ON CENTRAL SYSTOLIC BLOOD PRESSURE AND ARTERIAL STIFFNESS

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e354
Author(s):  
Elizabeth do Espirito Santo Cestari ◽  
Priscilla Galisteu de Mello ◽  
Tatiane de Azevedo Rubio ◽  
Maira Regina de Souza ◽  
Eliangela Gianini Gonzales ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Central Systolic Blood Pressure

scholarly journals Dysregulation of the Renin-Angiotensin System and Cardiometabolic Status in Mice Fed a Long-Term High-Fat Diet

2019 ◽  
Vol 25 ◽  
pp. 6605-6614 ◽  
Author(s):  
Nana Jin ◽  
Yu Wang ◽  
Lin Liu ◽  
Feng Xue ◽  
Tingbo Jiang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Renin Angiotensin System ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Açaí seed extract prevents the renin-angiotensin system activation, oxidative stress and inflammation in white adipose tissue of high-fat diet–fed mice

2020 ◽  
Vol 79 ◽  
pp. 35-49 ◽  
Author(s):  
Izabelle Barcellos Santos ◽  
Graziele Freitas de Bem ◽  
Cristiane Aguiar da Costa ◽  
Lenize Costa Reis Marins de Carvalho ◽  
Amanda Faria de Medeiros ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
Seed Extract ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
System Activation

Cardiovascular hypertrophy in diabetic spontaneously hypertensive rats: optimizing blockade of the renin–angiotensin system

2003 ◽  
Vol 104 (4) ◽  
pp. 341-347 ◽  
Author(s):  
Markus LASSILA ◽  
Belinda J. DAVIS ◽  
Terri J. ALLEN ◽  
Louise M. BURRELL ◽  
Mark E. COOPER ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Calcium Channel ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The aim of the present study was to compare the antihypertrophic effects of blockade of the renin–angiotensin system (RAS), vasopeptidase inhibition and calcium channel antagonism on cardiac and vascular hypertrophy in diabetic spontaneously hypertensive rats (SHR). SHR with streptozotocin-induced diabetes were treated with one of the following therapies for 32 weeks: the angiotensin-converting enzyme (ACE) inhibitor captopril (100mg/kg); the angiotensin AT1 receptor antagonist valsartan (30mg/kg); a combination of captopril with valsartan; the vasopeptidase inhibitor mixanpril (100mg/kg); or the calcium channel antagonist amlodipine (6mg/kg). Systolic blood pressure and cardiac and mesenteric artery hypertrophy were assessed. Mean systolic blood pressure in diabetic SHR (200±5mmHg) was reduced by captopril (162±5mmHg), valsartan (173±5mmHg), mixanpril (176±2mmHg) and amlodipine (159±4mmHg), and was further reduced by the combination of captopril with valsartan (131±5mmHg). Captopril, valsartan and mixanpril reduced heart and left ventricle weights by approx. 10%. The combination of captopril and valsartan further reduced heart weight (-24%) and left ventricular weight (-29%). Amlodipine did not affect cardiac hypertrophy. Only mixanpril and the combination of captopril and valsartan significantly reduced mesenteric weight. The mesenteric wall/lumen ratio was reduced by all drugs, and to a greater extent by the combination of captopril and valsartan. We conclude that optimizing the blockade of vasoconstrictive pathways such as the RAS, particularly with the combination of ACE inhibition and AT1 receptor antagonism, is associated with antitrophic effects in the context of diabetes and hypertension. In contrast, calcium channel blockade, despite similar effects on blood pressure, confers less antitrophic effects in the diabetic heart and blood vessels.

scholarly journals Increased (pro)renin receptor expression in the subfornical organ of hypertensive humans

2018 ◽  
Vol 314 (4) ◽  
pp. H796-H804 ◽  
Author(s):  
Silvana G. Cooper ◽  
Darshan P. Trivedi ◽  
Rieko Yamamoto ◽  
Caleb J. Worker ◽  
Cheng-Yuan Feng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Models ◽  
Systolic Blood Pressure ◽  
Renin Angiotensin System ◽  
Subfornical Organ ◽  
Antihypertensive Drug Therapy ◽  
Angiotensin System ◽  
Human Hypertension ◽  
Renin Angiotensin ◽  
The Brain

The central nervous system plays an important role in essential hypertension in humans and in animal models of hypertension through modulation of sympathetic activity and Na+ and body fluid homeostasis. Data from animal models of hypertension suggest that the renin-angiotensin system in the subfornical organ (SFO) of the brain is critical for hypertension development. We recently reported that the brain (pro)renin receptor (PRR) is a novel component of the brain renin-angiotensin system and could be a key initiator of the pathogenesis of hypertension. Here, we examined the expression level and cellular distribution of PRR in the SFO of postmortem human brains to assess its association with the pathogenesis of human hypertension. Postmortem SFO tissues were collected from hypertensive and normotensive human subjects. Immunolabeling for the PRR and a retrospective analysis of clinical data were performed. We found that human PRR was prominently expressed in most neurons and microglia, but not in astrocytes, in the SFO. Importantly, PRR levels in the SFO were elevated in hypertensive subjects. Moreover, PRR immunoreactivity was significantly correlated with systolic blood pressure but not body weight, age, or diastolic blood pressure. Interestingly, this correlation was independent of antihypertensive drug therapy. Our data indicate that PRR in the SFO may be a key molecular player in the pathogenesis of human hypertension and, as such, could be an important focus of efforts to understand the neurogenic origin of hypertension. NEW & NOTEWORTHY This study provides evidence that, in the subfornical organ of the human brain, the (pro)renin receptor is expressed in neurons and microglia cells but not in astrocytes. More importantly, (pro)renin receptor immunoreactivity in the subfornical organ is increased in hypertensive humans and is significantly correlated with systolic blood pressure.

High Fat Diet Exacerbates Neuroinflammation in an Animal Model of Multiple Sclerosis by Activation of the Renin Angiotensin System

2013 ◽  
Vol 9 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Silke Timmermans ◽  
Jeroen F. J. Bogie ◽  
Tim Vanmierlo ◽  
Dieter Lütjohann ◽  
Piet Stinissen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Animal Model ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin
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