Sodium kinetics in salt-sensitive and salt-resistant normotensive and hypertensive subjects

Molecular-Based Mechanisms of Mendelian Forms of Salt-Dependent Hypertension

“…The mechanisms whereby salt exacerbates hypertension may not reflect the mechanisms whereby salt initiates hypertension and could be influenced by the duration of pre-existing hypertension and other confounding factors that are difficult to ascertain. It should be noted that the results of hemodynamic and metabolic studies of dietary salt loading that compared salt-sensitive hypertensives versus saltresistant hypertensives 34,35 differ from the results of those that compared salt-sensitive normotensives versus salt-resistant normotensives. [28][29][30]35 It is also important to note that the saltloading study comparing salt-sensitive hypertensives versus salt-resistant hypertensives 34 did not include normal controls, ie, normotensive salt-resistant individuals.…”

“…It should be noted that the results of hemodynamic and metabolic studies of dietary salt loading that compared salt-sensitive hypertensives versus saltresistant hypertensives 34,35 differ from the results of those that compared salt-sensitive normotensives versus salt-resistant normotensives. [28][29][30]35 It is also important to note that the saltloading study comparing salt-sensitive hypertensives versus salt-resistant hypertensives 34 did not include normal controls, ie, normotensive salt-resistant individuals. Because that study did not include normal controls, it did not determine whether the cardiac output and sodium balance responses to salt loading were normal or abnormal in the salt-sensitive hypertensives or in the salt-resistant hypertensives.…”

“…A, Common pathway in normal nonmutant subjects that yields a normal (nonpressor) response to increases in salt (NaCl) intake within the range of usual daily salt intake observed in modern societies. In normal subjects, such nonextreme yet substantial increases in salt intake often induce substantial increases in salt retention 29,30,[35][36][37] and transient increases in cardiac output, 29,30 but typically do not initiate hypertension because potential pressor effects of even large salt-induced increases in cardiac output (CO; +10%) are normally offset by depressor effects of salt-induced decreases in systemic vascular resistance. 29,30 Systemic vascular resistance is conventionally defined as the combined resistance of the entire resistance vasculature.…”

“…However, when salt intake is increased, salt balance is not immediately achieved in normal individuals. Because of the delay in achieving salt balance in normal humans, increases in salt intake can cause substantial increases in body salt content 29,30,[35][36][37] and increases in CO. 29,30 In this pathway, salt-induced decreases in renal vascular resistance are held to (1) contribute to the salt-induced decreases in systemic vascular resistance that hemodynamically prevent salt-induced increases in CO from causing hypertension and (2) contribute to the achievement of salt balance by facilitating sodium excretion. Note that although this pathway is focused on the initiation phase of salt-loading, it also depicts changes in CO and systemic vascular resistance that transpire after the salt-induced increase in CO and the salt-induced decrease in systemic vascular resistance have occurred.…”

Salt sensitivity in hypertension. Renal and cardiovascular implications.

“…15 Others have shown a longer half-life of sodium balance in salt-sensitive compared with saltresistant patients despite no difference in salt retention. 30 Most studies have also been unable to show a statistically significant relation between the amount of sodium lost during depletion or retained during NaCl loading and changes in arterial pressure. 1 The slope of the renal function (pressure-natriuresis) curve is significantly lower in salt-sensitive than saltresistant patients (Fig I), 31 -32 suggesting a disturbance in renal tubular sodium reabsorption.…”