The aim of this paper was to review mechanistic links between excessive salt intake, systemic and tissue activation of the renin-angiotensin-aldosterone system (RAAS), and insulin resistance, and their contibution to the development of hypertension, cardiovascular disease (CVD) and chronic kidney disease (CKD). It has been reported that excess dietary salt and fat have a substantial influence on blood pressure elevation, but also on insulin resistance. The role of sodium appears to be mediated by activation of the sympathetic nervous system (SNS) as well as RAAS activation and signalling through the mineralocorticoid receptor (MR). These complex processes induce an oxidative stress, which contribute to insulin resistance and impaired vascular function leading to the development of hypertension, atherosclerosis, CKD and CVD. Moreover, it has been documented that salt restriction, as well as RAAS and MR blockade improve not only hypertension and CVD risk profile, but also insulin sensitivity and glucose homeostasis. This review supports the fact that salt sensitivity and insulin resistance are key elements responsible for the relationship between hypertension and type 2 diabetes and consequently CKD and CVD.
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