engleski

salt and renal vascular dysfunction

The most common environmental factor that contributes to the pathogenesis of hypertension is elevated dietary salt ingestion. It is well documented that high salt diet significantly affects the vascular function, leading to impaired vascular responses to various physiological and pharmacological stimuli, i.e. vasodilators and vasoconstrictors. The renal vasculature plays a major role in the regulation of renal blood flow and the ability of the kidney to control the plasma volume and blood pressure. Genetic and salt-sensitive hypertension is marked by renal vascular dysfunction, associated with renal vasoconstriction, increased vascular resistance, decreased renal blood flow, and consequent increase in plasma volume, and blood pressure. Although the mechanisms of dietary salt-induced hypertension and renal injury are still not clear, there is an increasing body of evidence that genetic mutations of sodium channels and related proteins, membrane ion transporter(s), and/or a regulatory enzyme in the nephron and renal vasculature are important in development of renal vascular dysfunction resulting in hypertension. In addition, vascular inflammation, and oxidative stress further promote renal vascular dysfunction, demonstrated as decrease in production/bioavailability of vasodilatory mediators (nitric oxide, prostaglandins, endothelium- derived hyperpolarizing factors) and/or increase in vasoconstrictors (such as tromboxane A2, endothelin, angiotensin II, 20-HETEs). Also, long-term HS diet induces renal injury and hypertension, which are associated with decreased renal VEGF expression. Modification of extracellular matrix composition could also lead to renal vascular remodeling and development of hypertension. In conclusion, reduction in dietary salt intake could be beneficiary in decreasing risk of renal damage and in management of hypertension.

dietary salt; hypertension; renal vascular function

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