A Novel Cell Volume Sensor for Real-Time Analysis of Ca-Activated K Channel.

Potassium channels play a vital role in cell volume regulation. A cell volume sensor was constructed by integrating regulatory volume decrease (RVD) with quartz-crystal microbalance (QCM) for studying potassium channels and their expression. The sensor successfully monitored the K channel's activities during RVD by sensitive and noninvasive means.

Renal Farnesoid X Receptor improves high fructose-induced salt-sensitive hypertension in mice by inhibiting DNM3 to promote nitro oxide production.

Objective: Farnesoid X Receptor (FXR) is highly expressed in renal tubules, activation of which attenuates renal injury by suppressing inflammation and fibrosis. However, whether renal FXR contributes to the regulation of blood pressure (BP) is poorly understood. This study aimed to investigate the anti-hypertensive effect of renal FXR on high-fructose-induced salt-sensitive hypertension and underlying mechanism.

Moderation of gut microbiota and bile acid metabolism by chlorogenic acid improves high-fructose-induced salt-sensitive hypertension in mice.

Chlorogenic acid (CGA) is a natural compound with many important pharmacological effects including anti-hypertension. This study aimed to investigate the anti-hypertensive effect of CGA on high-fructose-induced salt-sensitive hypertension and the underlying mechanism. Hypertension was induced in male C57BL/6 mice by 20% fructose in drinking water plus 4% sodium chloride in the diet (HFS) for 8 weeks.

Enterococcus faecalis contributes to hypertension and renal injury in Sprague-Dawley rats by disturbing lipid metabolism.

Objective: Increasing studies have demonstrated that gut microbiota play vital roles in the development of hypertension. However, the underlying mechanism is not fully understood.

Methods: The relative abundance of Enterococcus faecalis was determined in the faecal samples of angiotensin II or deoxycorticosterone acetate/salt-induced hypertensive rats.

Correction: ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Sodium butyrate ameliorates deoxycorticosterone acetate/salt-induced hypertension and renal damage by inhibiting the MR/SGK1 pathway.

Our recent work demonstrates that infusion of sodium butyrate (NaBu) into the renal medulla blunts angiotensin II-induced hypertension and improves renal injury. The present study aimed to test whether oral administration of NaBu attenuates salt-sensitive hypertension in deoxycorticosterone acetate (DOCA)/salt-treated rats. Uninephrectomized male Sprague-Dawley (SD) rats were treated with DOCA pellets (150 mg/rat) plus 1% NaCl drinking water for 2 weeks.

ELABELA attenuates deoxycorticosterone acetate/salt-induced hypertension and renal injury by inhibition of NADPH oxidase/ROS/NLRP3 inflammasome pathway.

ELABELA (ELA), a 32-residue hormone peptide abundantly expressed in adult kidneys, has been identified as a novel endogenous ligand for APJ/Apelin receptor. The aim of this study was to investigate the role of ELA in deoxycorticosterone acetate (DOCA)/salt-induced hypertension and further explore the underlying mechanism. In DOCA/salt-treated rats, the mRNA level of ELA greatly decreased in the renal medulla.

Gut dysbiosis contributes to high fructose-induced salt-sensitive hypertension in Sprague-Dawley rats.

Objectives: Although it is known that high fructose intake causes salt-sensitive hypertension, the underlying mechanism remains unclear. The aim of this study was to determine whether chronic intake of high fructose coupled with salt (HFS) might alter the structure of the gut microbiota, which contributes to elevated blood pressure.

Methods: For 8 wk, Sprague-Dawley rats were given 20% fructose in drinking water and 4% sodium chloride in their diet to induce hypertension.