High potassium diets reduce mortality and mesangial matrix expansion in diabetic rats. Diabetes shows endothelial dysfunction.

High K diets greatly reduce arterial and endothelial injury and mortality rate in hypertensive rats. Might they do so in normotensive diabetic rats? . Rats were injected with 41 mg/Kg streptozotocin; 74 became diabetic (serum glucose averaging 650 mg/dl). Forty two diabetic rats were fed a .45% normal K diet, while 32 other diabetic rats were fed a 1.25% high K diet, for 36 wks in both groups. After 12 wks on the two diets, the high K rats had a much better survival rate than the normal K rats. At 13 wks, 73% lower mortality in high K rats, p<.05. At 18 wks, 52% fewer deaths in high K rats, p<.05. At 24 wks, 56% fewer deaths in high K rats, p<.01. At 30 wks, 46% fewer deaths in high K rats, p<.01. At 36 wks, 39% fewer deaths in high K rats, p<.02. The mortality in high K rats was significantly lower during every week of this feeding period. Thus, just as we found that high K diets reduced mortality in Dahl S rats and SHRsp rats, they also significantly reduce deaths in diabetic rats. . Since high K diets greatly improve endothelial function in hypertensive rats, we wondered whether they would reduce mesangial matrix expansion characteristic of diabetic rats. For 8 months, 10 diabetic rats were fed a .45% normal K diet, while 11 other diabetic rats were fed a 1.25% high K diet. Using electron microscopy, in 7 non-diabetic control rats, the mesangial matrix averaged 37% of the total mesangium. In 11 diabetic rats on a normal K diet, the mesangial matrix occupied 54% of the mesangium, while in 10 diabetic rats on the high K diet, the mesangial matrix occupied only 48.6% of the mesangium, a 10% reduction (p<.02). Thus, the high K diet was associated with a reduction in the size of the mesangial matrix in the direction of normal. This effect could be related to improved health of glomerular endothelial cells, but more evidence is required. . Diabetic aortic rings in a bath (n=31) averaged 52% relaxation to 10−7 acetylcholine vs 75% in non-diabetics (n=25) (31% less in diabetics, p<.0001). Nitroprusside (10−7) relaxation was closely similar in both groups. These results suggest injured and dysfunctional endothelial cells in diabetes.