ELEVATED ERYTHROCYTE SODIUM-LITHIUM COUNTERTRANSPORT IN HYPERTENSIVE PATIENTS WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS

Citation
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
Citations number
32
Categorie Soggetti
Gastroenterology & Hepatology","Endocrynology & Metabolism
ISSN journal
01688227
Volume
31
Issue
1-3
Year of publication
1996
Pages
37 - 44
Database
ISI
SICI code
0168-8227(1996)31:1-3<37:EESCIH>2.0.ZU;2-S
Abstract
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.