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.
Highlights
The vascular system is a closed transport network with a rigid structure that contracts and relaxes
This system is divided into three major categories: veins, arteries, and capillaries
Between the intima and the adventitia lies the tunica media or media composed of abundant elastic fibers and contractile vascular smooth muscle cells (VSMCs), which control the vessel tone (Figure 1)
Summary
Intracellular free Ca2+ and Na+ are not homogeneously distributed in excitable and non-excitable cells [36,37,38]. It is known to be involved in the activation of chromatin [45] and nuclear pore functioning [38,46] This exchanger’s activity can directly affect gene expression and perinucleoplasmic, nucleoplasmic, and cytoplasmic homeostasis of Na+ and Ca2+ under normal and pathological conditions [37,38,43]. The NCX1 is a transmembrane protein that was cloned in 1990 and is expressed at the cytoplasmic membrane, nuclear membrane, and in the mitochondria of a variety of cells, such as hepatocytes, cardiomyocytes, endothelial cells, VECs, and VSMCs [37,43,48,49,50,51] It has an amino-terminal portion composed of 5 transmembrane domains and a carboxy-terminal portion consisting of 4 transmembrane domains [49,50]. This type of channel in VSMCs and VECs, and, more from the healthy human origin, is still a matter of debate because of the absence of a specific blocker of this channel
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