engleski

Salt and renin-angiotensin system

Numerous observational and experimental studies have confirmed the association of sodium intake with blood pressure levels. A high-salt diet is one of the major risk factors in the development and maintenance of hypertension. The renin-angiotensin system (RAS) is a key factor in many cases of essential hypertension, as indicated by the successful treatment of high blood pressure with angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers. Indeed, mutations in the renin gene (or other genes that encode components of the RAS) have been described in the development of hypertension and salt sensitivity. The RAS is a crucial homeostatic system that controls body fluid volume, electrolyte balance, blood pressure, and neuronal and endocrine functions related to cardiovascular control. The RAS exhibits its effects through the effector molecule angiotensin II, which binds to specific membrane-bound angiotensin receptors located in multiple tissues, including the vasculature. Endothelial dysfunction underlies hypertension and other cardiometabolic diseases. Endothelial function is impaired with high salt dietary intake prior to increases in blood pressure. Novel studies suggest that this impairment is related to suppressed levels of angiotensin II and that angiotensin II has permissive, modulatory effect on the mechanisms of endothelial function, including changes in oxidative- antioxidative balance, low-grade of inflammation and various vasodilatory and vasocontrictory pathways. Besides the mentioned effects of high sodium intake on the RAS, endothelial dysfunction and sympathetic nervous system activity, some other factors should also be considered as important contributors to the blood pressure increase linked to salt intake, including volume expansion (and elevated peripheral resistance in the later phase), functional changes of ion exchangers (such as the Na-Li countertransport) and possibly a reduced activity of the kallikrein-kinin system in the kidney.

NaCl, renin-angiotensin system, hypertension, microcirculation

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