Hypertension (HTN) accounts for 6% of death worldwide. The prevalence of HTN varies being lowest in rural India (3.4% in men and 6.8% in women), and highest in Poland (68.9% in men and 72.5% in women).1 Prevalence of HTN was 27.1% in men and 30.1% in women in the adult population of United States.
1HTN is a risk factor for cardiovascular diseases including stroke and myocardial infarction. There are two types of HTN. Primary or essential which accounts for 90 to 95% and its etiology is not known. Secondary HTN which accounts for 5 to 10% and its etiology is known.Advanced glycation end products (AGEs) and its cellular receptor (RAGE) may play a role in the pathophysiology of HTN. Interaction of AGEs with RAGE increases the expression and release of inflammatory cytokines, generation of reactive oxygen species (ROS), and activates nuclear factor kappa-B (NF-κB).2-4 These agents might affect the structures of arterial wall and/or produce contraction of the arterial wall. Various measures are available for the prevention and treatment of HTN. 5 However, very little attention has been given to the role of AGEs and its receptors in initiation and maintenance of arterial stiffness and HTN.
Keywords► advanced glycation end products ► receptor for AGE ► soluble receptor for AGE ► hypertension ► arterial stiffness ► management of hypertension
AbstractThere is a close relationship between arterial stiffness and blood pressure. The studies suggest that the advanced glycation end products (AGEs) and its cell receptor (RAGE) are involved in the arterial stiffness in two ways: changes in arterial structure and vascular function. Plasma levels of AGEs and expression of RAGE are elevated, while the levels of soluble RAGE (sRAGE) and endogenous secretory RAGE (esRAGE) are lowered in patients with hypertension (HTN). There is a positive correlation between plasma levels of AGEs and arterial stiffness, and an inverse association between arterial stiffness/HTN, and serum levels of sRAGE and esRAGE. Various measures can reduce the levels of AGEs and expression of RAGE, and elevate sRAGE. Arterial stiffness and blood pressure could be reduced by lowering the serum levels of AGEs, and increasing the levels of sRAGE. Levels of AGEs can be lowered by reducing the consumption of AGE-rich diet, short duration of cooking in moist heat at low temperature, and cessation of cigarette smoking. Drugs such as aminoguanidine, vitamins, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-II receptor blockers, statins, and metformin inhibit AGE formation. Alagebrium, an AGE breakers reduces levels of AGEs. Clinical trials with some drugs tend to reduce stiffness. Systemic administration of sRAGE has beneficial effect in animal studies. In conclusion, AGE-RAGE axis is involved in arterial stiffness and HTN. The studies suggest that inhibition of AGEs formation, reduction of AGE consumption, blockade of AGE-RAGE interaction, suppression of RAGE expression, and exogenous administration of sRAGE may be novel therapeutic strategies for treatment...