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Abnormalities in Na+/H+ antiporter activity in diabetic nephropathy
1Department of Pharmacology, Leicester Royal Infirmary, United Kingdom.
Journal of the American Society of Nephrology : JASN
|October 1, 1992
Summary
Increased cellular sodium-hydrogen (Na+/H+) antiport activity is linked to hypertension and may predispose individuals to essential hypertension. This membrane transport abnormality is also observed in type 1 diabetic patients with nephropathy, potentially contributing to kidney disease.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Cellular Biology
Background:
- Hypertension is associated with abnormalities in cellular transport mechanisms.
- Increased cellular Na+/H+ antiport activity is a known marker in hypertensive individuals and animal models.
- This membrane abnormality has implications for vascular structure and function.
Purpose of the Study:
- To investigate the role of cellular Na+/H+ antiport activity in hypertension.
- To explore the presence of this transport abnormality in type 1 diabetic nephropathy.
- To determine if this marker indicates a predisposition to essential hypertension and diabetic nephropathy.
Main Methods:
- Analysis of cellular Na+/H+ antiport activity in leukocytes, platelets, skeletal muscle, and vascular smooth muscle cells from hypertensive subjects and spontaneously hypertensive rats.
- Examination of leukocytes and fibroblasts from type 1 diabetic patients with nephropathy.
Main Results:
- Increased cellular Na+/H+ antiport activity was confirmed in various cell types in hypertensive models.
- A similar membrane transport abnormality was identified in leukocytes and fibroblasts of type 1 diabetic patients with nephropathy.
- Medial thickening of resistance vessels was associated with this membrane abnormality.
Conclusions:
- The cellular Na+/H+ antiport system is implicated in the pathophysiology of hypertension.
- This membrane transport marker may predict essential hypertension risk.
- The abnormality could contribute to the development of diabetic nephropathy, potentially via mesangial expansion.