Kinetic characteristics of the erythrocyte sodium-lithium countertransporter in subjects with coronary artery disease

Abstract

Sodium-lithium countertransport activity, external affinity for sodium (kNa) and maximal rate of turnover (Vmax), were characterized in 21 male subjects (aged 45 to 65 years) with angiographically proven coronary artery disease; these were compared with a matched group of healthy controls. No significant differences in countertransport activity were noted between the coronary artery disease patients and the healthy controls. By contrast, the median [range] kNa in the coronary artery disease group (8.5 [2.6 to 30.5] mmol/L Na) was significantly lower than that in the controls (59.9 [5.9 to 240.5] mmol/L Na; P < .0001). This reduction was accompanied by a significantly lower mean Vmax (controls 0.403 +/- 0.187 v coronary artery disease group 0.248 +/- 0.121 mmol Li/L RBC/h; P < .01). The findings suggest that disturbed behavior of the sodium-lithium countertransporter is not confined to hypertension but may represent a broader-based membrane dysfunction associated with vascular disease.

Effects of lipids in patients with familial hypercholesterolaemia on the kinetics of the sodium-lithium countertransporter

“…[1][2][3][4][5][6][7][8][9] However, our data do not show any relationship of SLC kinetic parameters with markers of insulin resistance. This relationship has been described as being absent in other normotensive populations.…”

“…1 Associations have been demonstrated with non-insulin dependent diabetes mellitus, 2 essential hypertension, [3][4][5] and risk of coronary artery disease. [6][7][8] The activity of SLC can be resolved into kinetic components of maximal turnover velocity (V max ) and substrate affinity (K m ). 1,2,9 Few studies have examined the inter-relationship of SLC kinetics and primary dyslipidaemia.…”

Kinetic characteristics of the erythrocyte sodium-lithium countertransporter in black normotensive subjects compared with three other ethnic groups

“…A lowered k Na has been proposed as a possible marker for predisposition to hypertension, 16,28 while we have found it to be linked with general vascular disease. 17 It is possible that the trend to lower k Na values in this group of young black subjects may have broader relevance if extrapolated to the finding of increased susceptibility to hypertension and vascular disease seen in larger black populations.…”

“…15 Studies which have characterised the countertransporter with respect to these two kinetic terms have suggested that it is an alteration in the affinity of the countertransporter for external sodium that accompanies hypertension and vascular disease and not a change in maximal velocity. 16,17 The aim of the present study was to investigate the kinetics of the sodium-lithium countertransporter in black normotensive subjects to identify the kinetic locus (k Na or V max ) responsible for the reduced activity noted in black populations. At the same time, behaviour of the sodium-lithium countertransporter in black and Caucasian subjects have been compared for the first time with countertransport behaviour in subjects of Chinese and South Asian extraction.…”

Sodium/lithium countertransport and intracellular calcium concentration in patients with essential hypertension and coronary heart disease

“…Thus a high intracellular calcium concentration ([Ca# + ] i ) and high activity of the Na + \H + exchanger have been reported to be associated with a high proliferation rate and growth of vascular smooth muscle cells [13,[20][21][22][23], as well as with left ventricular hypertrophy [24]. Furthermore, increased Na + \Li + CT activity has been shown to be associated with left ventricular hypertrophy [18,19,[24][25][26], coronary heart disease (CHD) [27], hyperlipidaemia [4,7,8] and urinary albumin excretion [1,18,28]. A relationship between Na + \Li + CT activity and diabetic nephropathy is less evident [4,29,30].…”