Urinary Potassium Excretion and Sodium Sensitivity in Blacks

Abstract

Abstract-Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle's loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure. Key Words: blacks Ⅲ hypertension, essential Ⅲ kidney Ⅲ potassium Ⅲ sodium B lood pressure of a subset of the human population rises as a result of an increase in the intake of salt (sodium chloride). 1 Individuals who manifest this trait are salt sensitive. As sodium (and chloride) balance must be preserved to sustain life, salt-sensitive and salt-resistant subjects maintain sodium balance. What distinguishes salt-sensitive from saltresistant subjects is that in the face of a high-salt intake, salt-sensitive subjects raise their blood pressure, ultimately maintaining sodium balance by resorting to pressure natriuresis. 2 However, a habitually high salt consumption in susceptible individuals may exert biological effects other than salt-evoked blood pressure elevation, including left ventricular hypertrophy, stiffness of conduit arteries, and stroke. [3][4][5] The kidneys are the main player in salt sensitivity, but mechanisms causing this trait are a matter of conjecture. Lessons from rare, monogenic forms of hypertension and hypotension arising from abnormalities in renal sodium handling 6 -8 suggest that salt sensitivity need not be a single entity; rather, it is probably a clinical manifestation of a number of renal disorders that result in altered electrolyte homeostasis and thus blood pressure elevation.Salt sensitivity in blacks has begged for a physiological explanation ever since the predilection of this group to essential hypertension and progressive renal damage has come to light. In a previous communication, we offered a paradigm that explains salt sensitivity in blacks. 9 This article further expands the model by proposing that the differences in renal potassium handling between blacks and whites reflect ethnic variation in the fractional reabsorption of sodium in specific renal tubular segments. Moreover, we propose that mechanisms in the renal regulation of sodium may explain the predisposition of blacks to sodium-induced elevation of blood pressure and also to sodium-induced glomerular damage. Here, we refer to salt sensitivity as "sodium sensitivity," albeit some research has suggested that not only sodium but also chloride, potassium, and perhaps other nutrients may contribute to the salt-sensitivity trait. 10 -13 Although irrefutable evidenc...

Hyperaldosteronism and Hypertension

“…35 We also observed that plasma sodium concentrations were lower in the blacks. Also consistent with previous observations of others, 36 in the current study, plasma AVP concentrations were higher in the blacks, and conceivably this may account for the lower serum sodium concentrations.…”

Common variants of the UMOD promoter associated with blood pressure in a community-based Chinese cohort

“…18,19 Aviv et al 20,21 reviewed previously reported clinical studies that indicated that the thick ascending limb (TAL) had a pivotal role in the susceptibility of Blacks to HTN. A mechanism was proposed in which an increase in NKCC2 activity could lead to the expansion of the extracellular volume and thus be associated with HTN.…”

“…The common variants of the UMOD promoter will influence the mRNA level and thus regulate the expression/ secretion of UMOD in the renal TALs. The renal TALs have important roles in sodium reabsorption, 20,21 and UMOD may regulate sodium reabsorption in this tissue 24 and thus regulate BP. One of our results appeared to be contradicted by previous studies, indicating that the real mechanism of UMOD in the regulation of BP needs to be further explored.…”

Potassium Chloride Supplementation Diminishes Platelet Reactivity in Humans

“…This topic is addressed in detail in a recent communication. 16 The mechanism that accounts for the effect of potassium supplementation on ADP-evoked platelet aggregation is unclear. We suspect that this phenomenon may ultimately relate to the link between the sodium/potassium gradients across the platelet plasma membrane and platelet cytosolic calcium, which is the penultimate platelet activator.…”