High Na+ Salt Diet and Remodeling of Vascular Smooth Muscle and Endothelial Cells

Abstract

Our knowledge on essential hypertension is vast, and its treatment is well known. Not all hypertensives are salt-sensitive. The available evidence suggests that even normotensive individuals are at high cardiovascular risk and lower survival rate, as blood pressure eventually rises later in life with a high salt diet. In addition, little is known about high sodium (Na+) salt diet-sensitive hypertension. There is no doubt that direct and indirect Na+ transporters, such as the Na/Ca exchanger and the Na/H exchanger, and the Na/K pump could be implicated in the development of high salt-induced hypertension in humans. These mechanisms could be involved following the destruction of the cell membrane glycocalyx and changes in vascular endothelial and smooth muscle cells membranes’ permeability and osmolarity. Thus, it is vital to determine the membrane and intracellular mechanisms implicated in this type of hypertension and its treatment.

Early Low-Grade Inflammation Induced by High-Salt Diet in Sprague Dawley Rats Involves Th17/Treg Axis Dysregulation, Vascular Wall Remodeling, and a Shift in the Fatty Acid Profile

“…Namely, complete proteome analysis of the brain blood vessel tissue is indicative of an ongoing tissue remodeling process and perturbations in the energy metabolism induced by HSD. This is in accordance with the previous finding of sodium-induced impairment of the endothelial glycocalyx contributing to endothelial cell stiffening and subsequent endothelial dysfunction [44][45][46], as well as the finding of long-term salt loading induced vascular remodeling and cardiac fibrosis in strokeprone spontaneously hypertensive rats [47].…”

Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy

“…It was found that six weeks of moderate-intensity exercise training reduced the expression of CaMKII and allowed more effective control of glucose homeostasis by improving glucose uptake in adipose and muscle tissue [ 138 ]. Another study reported that a chronically high salt intake induced an increase in intracellular ROS and high CaMKII activity which led to impaired endothelial function [ 139 ]. Studies in obese individuals show that adipocytes have higher intracellular mitochondrial Ca 2+ levels and reduced glucose uptake [ 140 ].…”

Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications

“…Through integration with various cellular processes, integrins become indispensable in regulating cell functions such as inflammation, proliferation, migration, adhesion, and differentiation. The dysregulation of integrin signaling and conduction can lead to a variety of pathophysiological mechanisms, ultimately contributing to the initiation and progression of CVDs [165]. In the context of AS, integrins can orchestrate plaque formation by promoting EC oxidative stress and inflammation activation, recruiting and promoting the proliferation of VSMCs, inducing calcification, and allowing for the infiltration of immune cells and platelets [15,35,44,62].…”