T. Senda et al., ELEVATED ERYTHROCYTE SODIUM-LITHIUM COUNTERTRANSPORT IN HYPERTENSIVE PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS, Diabetes research and clinical practice, 31(1-3), 1996, pp. 37-44
Increased erythrocyte (RBC) sodium-lithium (Na-Li) counter transport (
CT) has been reported to be a genetic marker for essential hypertensio
n (EHT). In addition, increased RBC Na-Li CT has been demonstrated in
insulin-dependent diabetic (IDDM) patients with nephropathy, indicatin
g that a predisposition to hypertension may cause renal damage and imp
aired renal function. Therefore, the present study was designed to det
ermine RBC Na-Li CT in subjects with essential hypertension (EHT) and
non-insulin-dependent diabetics (NIDDM) with or without hypertension (
NIDDMHT or NIDDMNT), using the method of Canessa et al. with a slight
modification by flame photometry and expressed as nmol Li/5 x 10(6) RB
C/h. Na-Li CT in patients with EHT (0.159 +/- 0.051 (S.D.), n = 26) or
NIDDMHT (0.168 +/- 0.083, n = 42) was higher than that in NIDDMNT pat
ients (0.127 +/- 0.059, n = 27, P < 0.05). Among the NIDDMHT patients,
those with clinical nephropathy had the same levels of Na-Li CT as th
ose without nephropathy. When the NIDDM patients were divided into two
groups with or without insulin treatment, the Na-Li CT in hypertensiv
es was higher than that in normotensives, irrespective of whether or n
ot they were on insulin therapy. Addition of insulin to RBCs in vitro
did not augment the Na-Li CT activity. These results suggest that an i
ncrease of Na-Li CT may not be due to the stimulatory effect of endoge
nous or exogenous insulin, and reflect a genetic predisposition for hy
pertension, and hence diabetic nephropathy, not only in IDDM but also
NIDDM patients.