Salt sensitivity in hypertension. Renal and cardiovascular implications.

Abstract

The mechanisms responsible for the increase in blood pressure response to high salt intake in salt-sensitive patients with essential hypertension are complex and only partially understood. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for such patients to retain salt and develop salt-dependent hypertension. The possible role of vasodilator and natriuretic agents, such as the prostaglandins, endothelium-derived relaxing factor, atrial natriuretic factor, and kinin-kallikrein system, requires further investigation. An association between salt sensitivity and a greater propensity to develop renal failure has been described in certain groups of hypertensive patients, such as blacks, the elderly, and those with diabetes mellitus. Salt-sensitive patients with essential hypertension manifest a deranged renal hemodynamic adaptation to a high dietary salt intake. During a low salt diet, salt-sensitive and salt-resistant patients have similar mean arterial pressure, glomerular filtra-D espite extensive research, controversy still exists regarding the role of dietary salt (NaCI) in hypertension.

Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats with and without Azotemia and in Response to Treatment with Amlodipine Besylate

“…Studies suggest that hypertensive black patients have significantly lower PRA than their white counterparts and demonstrate a disproportionately increased PAC 30, 31, 32. Such patients have a greater propensity to target organ damage and demonstrate a better response to antihypertensive agents such as calcium channel blockers and diuretics than those targeting the RAAS 33, 34. However, the role of activation of the RAAS in salt‐sensitive hypertension in black human patients is currently debated 35.…”

Endothelial nitric oxide synthase polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

“…Both genetic and environmental factors interact to determine the BP response to changes in salt intake. 1,[38][39][40] Experimental evidence indicates that NO plays a key role in endothelial health and salt sensitivity. 41 In genetic models of salt sensitivity and in human subjects, salt sensitivity appears linked to impaired NO production, [2][3][4][5][6] an effect reversed by administration of the NO precursor, L-arginine.…”

“…1 Nitric oxide (NO) has been shown to play a role in intrarenal haemodynamics, sodium homeostasis and salt-sensitive hypertension. In animal models and in human subjects, salt sensitivity has been shown to be linked to impaired NO production.…”

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

“…[1][2][3][4][5] Although the pathogenesis of salt sensitivity is unknown, both genetic and environmental factors appear to interact to determine the exaggerated BP response to changes in salt intake. [6][7][8][9][10][11][12][13][14][15] Increased reactivity of BP to salt is commonly observed in subjects with obesity and associated cardiovascular risk factors.…”