Sodium-Lithium Countertransport in Erythrocytes of Hypertension Prone Families in Utah

Williams, Roger R.; Hunt, Steven C.; Kuida, Hiroshi; Smith, Jean B.; Ash, K O

doi:10.1093/oxfordjournals.aje.a113640

Cited by 90 publications

(32 citation statements)

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“…Correlations of sodium-lithium countertransport with age, 17 measures of body size, 18 and plasma lipid levels 5 have been reported in previous studies. However, because samples for these studies were small or were ascertained through referral clinics or hospitals, the role of these concomitant traits in predicting sodium-lithium countertransport in the general population has remained uncertain.…”

Section: Discussionsupporting

confidence: 67%

Sodium-lithium countertransport and hypertension in Rochester, Minnesota.

Turner

Michels

1991

Hypertension

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The objectives of the present study were to determine whether increased sodium-lithium countertransport is associated with essential hypertension in the general Caucasian population and to determine whether this association is independent of the effects of gender, age, body size, and plasma lipids. We studied 543 men and 589 women from the population of Rochester, Minnesota. Mean sodium-lithium countertransport was higher in hypertensive than in normotensive subjects in men (370±147 [mean±SD] versus 315±110 jtmol/1 red blood cells [RBC]/hr, p<0.001) and in women (339±114 versus 269±92 fimol/l RBC/hr, /><0.001). Interindividual differences in plasma triglycerides, body mass index (wt/[ht]2 ), and plasma total cholesterol explained 13.0% of sodium-lithium countertransport variation in men (/><0.001) and 20.2% in women (/><0.001). Age did not predict additional sodium-lithium countertransport variation in either gender. Slopes of the regressions of sodium-lithium countertransport on plasma triglycerides, body mass index, and plasma total cholesterol did not differ between diagnostic groups in men (p=03l) or in women (p=0J29). After adjustment to remove sodium-lithium countertransport variation attributable to these covariates, mean sodium-lithium countertransport remained significantly higher in hypertensive than in normotensive subjects in men (354±139 versus 319±104 /i.mol/1 RBC/hr, p<0.01) and in women (311 ±103 versus 278±83 /imol/1 RBC/hr, p<0.01). These findings in a large sample from Rochester, Minnesota, support the conclusions that increased sodium-lithium countertransport is associated with essential hypertension in the general Caucasian population and that this association is independent of the effects of gender, age, body size, and plasma lipids. Additional studies are necessary to establish whether sodium-lithium countertransport is an independent predictor of risk of developing essential hypertension. {Hypertension 1991;18:183-190) S odium-lithium countertransport has been proposed as an indicator of inherited predisposition to essential hypertension. This proposal is based on the finding of higher mean sodium-lithium countertransport in Caucasian patients with hypertension and in their young, hypertensive-prone offspring than in selected normotensive controls.1 However, since the samples for most previous studies were small and were ascertained through referral clinics or hospitals, their findings may not be representative of the community at large. Furthermore, many characteristics other than blood pressure differ between hypertensive and normotensive individuals, and some of these vari-

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Section: Discussionsupporting

confidence: 67%

Sodium-lithium countertransport and hypertension in Rochester, Minnesota.

Turner

Michels

1991

Hypertension

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“…1 - 3518 The V max of this transporter in erythrocytes is familially aggregated. 367 Studies performed in twins, 45 families living in Utah, 4 and a sample of the general population in Rochester, Minnesota 20 have estimated that as much as 80-90% of the individual variance of the countertransporter can be accounted for by heritability.…”

Section: Discussionmentioning

confidence: 99%

Red blood cell lithium-sodium countertransport in non-modulating essential hypertension.

et al. 1989

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Abnormalities in erythrocyte Li-Na countertransport have been reported in hypertensive subjects, and the available evidence favors familial aggregation and striking heritability of this marker. It is uncertain, however, whether the abnormalities are associated with hypertension per se or whether they may be concentrated in a particular subset of hypertensive subjects. In the present study, maximal rates of Li-Na countertransport were measured in red blood cells of 82 white subjects, including 37 normotensive subjects and 45 normal-or high-renin hypertensive subjects previously classified as non-modulators (n=21) or modulators (n=24). Mean countertransport activity was significantly higher in non-modulators compared with normally modulating hypertensive or normotensive subjects (0.475±0.044 vs. 0.309±0.028 or 0.249+0.012 mmol/1 cellxhr, respectively, p<0.001). Modulators did not differ significantly from normotensive subjects with regard to mean countertransport activity. Red blood cell sodium pump and Na-K-Cl cotransport were not significantly different in modulating and non-modulating hypertensive subjects. These relations remained unchanged after adjusting for age, body weight, and plasma cholesterol levels by analysis of covariance. A countertransport value exceeding 0.50 mmol/1 cellxhr occurred in 40% of the non-modulators but in only one of the other subjects. In contrast, while one half of the modulators and normotensive subjects had a countertransport value less than 0.235 mmol/1 cellxhr, none of the non-modulators did. Thus, elevated countertransport appears to aggregate in the non-modulating subset of essential hypertensive subjects. If these findings are cautiously applied, selecting patients with an elevated countertransport activity (>0.50 mmol/1 cellxhr) may serve as a useful method for enriching a sample of the essential hypertensive population with patients who have the non-modulation trait. (Hypertension 1989;13:721-726)

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“…We did not find a significant increase in countertransport activity in this group of hypertensive subjects, perhaps because weight, which may affect countertransport, 28 ' 31 -34 was well matched in our normotensive and hypertensive groups. We have previously reported a correlation between total vascular resistance and RBC Li + -Na + countertransport activity, 18 but we did not observe any significant relationship between RBC countertransport and FVR over the wide range of conditions studied, perhaps because vascular structure differs between vascular beds.…”

Section: Discussionmentioning

confidence: 52%