Red-cell sodium-lithium countertransport and fractional excretion of lithium in normal and hypertensive humans.

Abstract

To examine the relations between erythrocyte sodium-lithium countertransport and renal proximal tubular sodium handling, we measured countertransport, and then subjected 30 normal and 32 hypertensive subjects, both white and black, to provocative maneuvers of volume expansion and contraction. The fractional excretions of sodium and lithium were measured simultaneously. In agreement with previous studies, we found that countertransport in erythrocytes was elevated in hypertensive patients compared with normal subjects. We also observed that whites have a higher level of countertransport than blacks. In the basal state, we found that fractional sodium excretion of hypertensive patients was no different than in normal subjects, whereas the fractional lithium excretion of hypertensive persons was increased compared with normotensive values. Volume expansion with 21 0.9% saline administered intravenously during a 4-hour period provoked an exaggerated natriuresis and a greater increase in fractional lithium clearance in hypertensive patients compared with the control group. With volume expansion and contraction, fractional lithium clearance and countertransport were directly correlated. Our data suggest that hypertensive persons do not have increased proximal tubular sodium reabsorption compared with normal subjects. Further, the exaggerated natriuresis of hypertension is, in part, the result of increased distal solute delivery. The fact that our hypertensive patients were older may partially explain the discrepancies between this report and previous observations. (Hypertension 1989;13:206-212)

A Missing Link Between a High Salt Intake and Blood Pressure Increase

“…Moreover, volume expansion caused a greater natriuresis and greater increase in fractional excretion of lithium among the hypertensive patients. It is suggested that hypertensive patients do not have increased proximal tubular sodium reabsorption and that the exaggerated natriuresis often observed in hyper-tension is a result of increased distal tubular sodium delivery (34). These conclusions were also confirmed in another paper (35).…”

“…The hypertensive patients had an increased Na + -Li + CT. The fractional excretion of lithium was higher in those with elevated BP, despite similar baseline values for the fractional excretion of sodium between normotensive and hypertensive individuals (34). Moreover, volume expansion caused a greater natriuresis and greater increase in fractional excretion of lithium among the hypertensive patients.…”

Sodium-lithium countertransport and cardiorenal abnormalities in essential hypertension.

“…25 Significant correlations between lithium clearance and rates of Na + -Li + countertransport have been reported by some authors in young patients with essential hypertension 10 and in the offspring of hypertensive patients 11 but have not been confirmed by other workers. 44 - 45 The discrepancies between these studies could be accounted for, at least in part, by differences in age, race, and clinical characteristics of the patients studied. Although caution must be used in the interpretation of lithium clearance, our findings support the view that hypertensive patients with high Na + -Li + countertransport reabsorb more sodium, which could explain their expanded sodium pool.…”

Blood Pressure in Relation to Interactions Between Sodium Dietary Intake and Renal Handling

“…16,[20][21][22][23][24] Weder first reported that 14 untreated hypertensive patients had a lower FE Li than 31 normotensive subjects (13.96% versus 17.75%; P<0.01). 20 In a later study, Burnier et al found that 13 untreated whitecoat hypertensive patients but not 53 untreated hypertensive patients had significantly lower FE Li than 48 normotensive subjects (11.6% versus 15.4% versus 17.0%).…”