A6369 TRPV1 Activation Attenuates High-Salt Diet-Induced Vascular Fibrosis Via Inhibition Of TGF-β1 Signaling

2018 ◽  
Vol 36 ◽  
pp. e25-e26
Author(s):  
Liu Chan ◽  
Shang Qian-Hui
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Tgf Β1

scholarly journals Early Passive Leg Movement Prevents Against the Development of Heart Failure With Preserved Ejection Fraction in Rats

2021 ◽  
Vol 8 ◽  
Author(s):  
Jian Liu ◽  
Xi-xin Ji ◽  
Yang Fu ◽  
Wen-chao Zhang ◽  
Hui-fang Ji ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Vessel ◽  
Signaling Pathway ◽  
High Salt ◽  
Preserved Ejection Fraction ◽  
High Salt Diet ◽  
Salt Diet ◽  
Leg Movement ◽  
Early Passive ◽  
Tgf Β1

Exercising was reported by several studies to bring great benefits to heart failure with preserved ejection fraction (HFpEF), which reduced the hospitalization and the mortality of heart failure. However, the underlying mechanism of exercising on HFpEF remains unclear. In the present study, we designed and constructed a device that can perform early passive leg movement (ePLM) in rats and further observed whether treatment of ePLM exerts protective effects on HFpEF of rats. Rats were fed with high salt feed to establish an animal model of pre-clinical diastolic dysfunction (PDD), which would eventually develop into HFpEF, and then treated rats with ePLM. We conducted several experiments to evaluate the conditions of heart and blood vessel. The results show that diastolic functions of heart and blood vessel in rats were significantly improved by treatment of ePLM. We also found that pathological injuries of heart and blood vessel were ameliorated after treatment of ePLM. Moreover, treatment of ePLM decreased the protein levels of Collagen type I, Collagen type III, MMP2, and MMP9 in heart and blood vessel, indicating that cardiac and vascular fibrosis were reduced apparently by treatment of ePLM. Further investigation suggested that treatment of ePLM probably inhibit the activation of TGF-β1/Smad3 signaling pathway as well as promote the activation of Akt/eNOS signaling pathway in high salt diet induced HFpEF. In conclusion, treatment of ePLM alleviated high salt diet induced HFpEF by inhibiting fibrosis via suppressing TGF-β1/Smad3 signaling pathway as well as activating Akt/eNOS signaling pathway, implicating treatment of ePLM as a promising novel non-pharmacological approach for HFpEF.

scholarly journals Sacubitril/Valsartan Reduces Fibrosis and Alleviates High-Salt Diet-Induced HFpEF in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Wenchao Zhang ◽  
Jianwei Liu ◽  
Yang Fu ◽  
Huifang Ji ◽  
Zheyan Fang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Signaling Pathway ◽  
High Salt ◽  
Angiotensin Receptor ◽  
High Salt Diet ◽  
Salt Diet ◽  
Neprilysin Inhibitor ◽  
Tgf Β1

Previous studies have confirmed the clinical efficacy of sacubitril/valsartan (Sac/Val) for the treatment of heart failure with reduced ejection fraction (HFrEF). However, the role of Sac/Val in heart failure with preserved ejection fraction (HFpEF) remains unclear. Sac/Val is a combination therapeutic medicine comprising sacubitril and valsartan that acts as a first angiotensin receptor blocker and neprilysin inhibitor (angiotensin-receptor neprilysin inhibitor (ARNI)). Here, we investigated the role of Sac/Val in high-salt diet-induced HFpEF coupled with vascular injury as well as the underlying mechanism. Rats were fed with high-salt feed, followed by intragastric administration of Sac/Val (68 mg/kg; i.g.). The results of functional tests revealed that a high-salt diet caused pathological injuries in the heart and vascular endothelium, which were significantly reversed by treatment with Sac/Val. Moreover, Sac/Val significantly decreased the levels of fibrotic factors, including type I collagen and type Ⅲ collagen, thus, reducing the ratio of MMP2/TIMP2 while increasing Smad7 levels. Further investigation suggested that Sac/Val probably reversed the effects of high-salt diet-induced HFpEF by inhibiting the activation of the TGF-β1/Smad3 signaling pathway. Thus, treatment with Sac/Val effectively alleviated the symptoms of high-salt diet-induced HFpEF, probably by inhibiting fibrosis via the TGF-β1/Smad3 signaling pathway, supporting the therapeutic potential of Sac/Val for the treatment of HFpEF.

463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 463-P
Author(s):  
TOMONORI KIMURA ◽  
YOSHITAKA HASHIMOTO ◽  
TAKAFUMI SENMARU ◽  
EMI USHIGOME ◽  
MASAHIDE HAMAGUCHI ◽  
...  
Keyword(s):  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

2019 ◽  
Vol 20 (14) ◽  
pp. 3495 ◽  
Author(s):  
Yanling Yan ◽  
Jiayan Wang ◽  
Muhammad A. Chaudhry ◽  
Ying Nie ◽  
Shuyan Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Significant Rise ◽  
Protein Carbonylation ◽  
High Salt ◽  
Kidney Cortex ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

scholarly journals High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries

Hypertension ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 853-859 ◽  
Author(s):  
Magdalena Gonzalez ◽  
Lorena Lobos ◽  
Felipe Castillo ◽  
Lorna Galleguillos ◽  
Nandy C. Lopez ◽  
...  
Keyword(s):  
High Salt ◽  
Resistance Arteries ◽  
High Salt Diet ◽  
Salt Diet ◽  
Angiotensin Type 2 Receptor ◽  
Angiotensin Type

Endothelin B receptors impair baroreflex function and increase blood pressure variability during high salt diet

2021 ◽  
pp. 102796
Author(s):  
Bryan K. Becker ◽  
Jermaine G. Johnston ◽  
Carolyn Young ◽  
Alfredo A. Torres Rodriguez ◽  
Chunhua Jin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Variability ◽  
High Salt ◽  
Increase Blood Pressure ◽  
High Salt Diet ◽  
Salt Diet ◽  
Baroreflex Function ◽  
Endothelin B

Effect of a high-salt diet on oxidant enzyme activity in skeletal muscle microcirculation

2002 ◽  
Vol 282 (2) ◽  
pp. H395-H402 ◽  
Author(s):  
Deborah M. Lenda ◽  
Matthew A. Boegehold
Keyword(s):  
Skeletal Muscle ◽  
Xanthine Oxidase ◽  
Salt Intake ◽  
Normal Diet ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Arteriolar Wall ◽  
Xanthine Oxidase Inhibition ◽  
Alternate Source

Increased salt intake attenuates the endothelium-dependent dilation of skeletal muscle arterioles by abolishing local nitric oxide (NO) activity. There is evidence of oxidative stress in arteriolar and venular walls of rats fed a high-salt diet, and depressed arteriolar responses to acetylcholine (ACh) in these rats are reversed by scavengers of reactive oxygen species (ROS). In this study, we tested the hypothesis that this salt-dependent increase in microvascular ROS and the resulting attenuation of endothelium-dependent dilation are due to increased expression and/or activity of oxidant enzymes in the microvascular wall. Resting arteriolar and venular wall oxidant activity, as assessed by tetranitroblue tetrazolium reduction, was consistently higher in the spinotrapezius muscle of rats fed a high-salt diet (7% NaCl, HS) for 4–5 wk than in those fed a normal diet (0.45% NaCl, NS) for the same duration. Western analysis of protein from isolated microvessels showed no difference between HS and NS rats in the expression of NAD(P)H oxidase or xanthine oxidase. Inhibition of NAD(P)H oxidase and/or xanthine oxidase with diphenyleneiodonium chloride and oxypurinol, respectively, reduced resting arteriolar wall oxidant activity to normal levels in HS rats but had no effect in NS rats, suggesting that the basal activities of NAD(P)H oxidase and xanthine oxidase are increased in HS microvessels. However, inhibition of these enzymes in HS rats did not restore normal arteriolar responses to ACh, suggesting that this stimulus activates an alternate source of ROS that eliminates the role of NO in the subsequent dilation.

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