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Hypertension Journal
Abstract
 
 

ABSTRACT

Enough evidence is there to link excess salt intake with cardiovascular and renal risks through hypertension though substantial evidence is also there to support that blood pressure is not always responding to salt. A lot of metabolic and neurohormonal factors determine this salt sensitivity in addition to genetic factors that determine substantial excretion of salt, so it may not increase blood pressure despite high intake. Salt-sensitive hypertensives have reduced levels of urinary endothelin, contributing to impaired natriuresis in response to a salt load. Salt load also increases free radicals and paradoxically decreases excretion of nitric oxide metabolites in salt-sensitive individuals. Type 2 diabetic patients with microalbuminuria are more salt sensitive as they have lower urinary excretion of nitric oxide. Nitric oxide deficiency facilitates endothelial dysfunction causing hypertension in salt-sensitive people, impeding vasodilation after salt load. Sympathetic nervous system plays a significant role in maintenance of blood pressure in response to salt through urinary and plasma levels of catecholamine and renal nerve activity. Apart from this, atrial natriuretic peptides (ANPs) and cytochrome P450-derived metabolites of arachidonic acid play significant roles. Insomnia and menopause increase salt sensitivity. Kidney provides sensitive and specific biomarkers for salt sensitivity in the form of proteomics, and renal proximal tubule cells, microribonucleic acid (miRNA), and exosomes are excreted into the urine apart from genetic biomarkers. A J-shaped curve relationship exists between salt intake and mortality. Salt intakes above and below the range of 2.5 to 6.0 gm/day are associated with high cardiovascular risk. Salt restriction can be a cause of hypertension in inverse salt-sensitive people. Available prevalence studies do not differentiate between salt-sensitive and salt-resistant populations, nor do they include normotensive salt-sensitive people who get their blood pressure raised in response to dietary salt. In these circumstances, salt sensitivity arises as an independent risk factor for cardiovascular mortality and morbidity.

Keywords: Dietary salt, Hypertension, Salt sensitivity.

How to cite this article: Maheshwari A, Basera H. Salt Sensitivity and Hypertension. Hypertens J 2017;3(4):178-182.

Source of support: Nil

Conflict of interest: None

 
 
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