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(Hypertension. 2008;52:188.)
© 2008 American Heart Association, Inc.
Brief Reviews |
From the Department of Physiology, Medical College of Georgia, Augusta.
Correspondence to Michael W. Brands, Department of Physiology, CA-3098, Medical College of Georgia, Augusta, GA 30912-3000. E-mail mbrands@mcg.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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In this framework, decreased GFR in diabetic nephropathy is responsible for imparting a chronic sodium-retaining influence on the kidneys, and hypertension is the counterbalancing natriuretic influence required to maintain sodium balance and sustain life. It, therefore, becomes curious that the early stages of diabetes are characterized by increased GFR and sodium balance, yet blood pressure is normal rather than low. For sodium balance to be maintained at normal blood pressure in the face of the chronic natriuretic influence of elevated GFR, there must be a concurrent sodium-retaining influence. If not, then the natriuretic effect of increased GFR would act unopposed and result in the maintenance of sodium balance at a lower blood pressure, similar to the effect of a diuretic. However, the
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