engleski

High sodium dietary intake and modulatory mechanism of sympathetic and immune system interactions

Increased dietary salt (NaCl) intake has been unequivocally linked to the development of hypertension and generally recognized as a risk factor for cardiovascular disease. One of the proposed mechanisms is genetically determined impaired renal salt handling capacity in the “salt-sensitive individuals”. Several mechanisms contribute to the hypertensive effect of dietary salt including increased water and sodium retention with resultant blood volume expansion, vascular abnormalities, neurogenicallymediated increases in peripheral resistance and activation of the immune cells that promote inflammation, oxidative stress and tissue damage. Excessive dietary salt intake leads to endogenous production of natriuretic substances (also known as cardiotonic steroids) resulting in inhibition and signalling of Na/K-ATPase in the cells of proximal renal tubules. Vasopressin neurons have an important role in coordinating neuroendocrine and autonomic responses to maintain cardiovascular homeostasis. High dietary salt intake increases the expression and activity of enpithelial Na- channels resulting in the steady state depolarization of vasopressin neurons. Similarly, dietary salt enhances the excitability of sympathetic neurons in the rostral ventrolateral medulla responsible for basal sympathetic vasomotor tone and critical for several sympathetic reflexes. These changes lead to increase peripheral vascular resistance and activation of the immune system that further promote end organ damage and maintain hypertension.

high salt diet ; immune system ; inflammation ; sympathetic system

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