Salt Sensitivity Hypertension and Lens Opacities

The number of patients with hypertension (HT) worldwide is estimated to reach 1.56 billion by 2025.HT accounts for almost 50% of deaths due to stroke and coronary artery disease. Salt-sensitive hypertension (SSH) accounts for about the half of all HT cases. Na+ /K+-ATPase activity is impaired in patients with SSH . Impaired Na+ /K+-ATPase activity in the lens epithelium results in cortical opacities in the peripheral equatorial region of the lens.A definite diagnosis of salt sensitivity is difficult, expensive, and associated with low patient compliance. Salt sensitivity is a risk factor for cardiovascular mortality and morbidity regardless of blood pressure and for other diseases such as asthma, gastric carcinoma, osteoporosis, and renal dysfunction. The present study is the first to investigate the potential of using lens opacity to predict SSH.

The transparency of the whole lens is largely based on epithelial cell permeability and Na+ /K+-ATPase activity. Circulation is activated by Na+ /K+-ATPases, which are present at 20-fold normal concentrations, particularly in the equatorial than in the anterior epithelial cells.

The mechanisms associated with SSH pathogenesis, such as signaling pathways involving Src family kinase (SFK), endothelin, connexin, brain natriuretic peptide (BNP), aldosterone, transient receptor protein V4 (TRPV4) ion channel, with-no-lysine kinase-Ste20-like proline/alanine rich kinase/oxidative stress-responsive kinase 1 (WNK-SPAK/OSR1), and Ras-related C3 botulinum toxin substrate (Rac1) , are important to the physiology of the lens epithelium. Compelling studies suggest that inhibition of these pathways may facilitate opacity.