Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2008;52:188-194
Published online before print July 7, 2008, doi: 10.1161/HYPERTENSIONAHA.107.090647
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
52/2/188    most recent
HYPERTENSIONAHA.107.090647v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brands, M. W.
Right arrow Articles by Labazi, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brands, M. W.
Right arrow Articles by Labazi, H.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Diabetes
*Diabetes Type 1
Hazardous Substances DB
*SODIUM
Related Collections
Right arrow Cardio-renal physiology/pathophysiology
Right arrow ACE/Angiotension receptors
Right arrow Animal models of human disease
Right arrow Other hypertension
Right arrow Type 1 diabetes
Right arrow Endothelium/vascular type/nitric oxide

(Hypertension. 2008;52:188.)
© 2008 American Heart Association, Inc.


Brief Reviews

Role of Glomerular Filtration Rate in Controlling Blood Pressure Early in Diabetes

Michael W. Brands; Hicham Labazi

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
 
Perhaps the most obvious, and least contentious, examples of hypertension caused by the kidneys are renal artery stenosis and diabetic nephropathy, because there are readily identifiable, physical limitations in the ability of the kidneys to excrete sodium in each case. The former is characterized by a global restriction in renal perfusion, and the latter is characterized more specifically by glomerular injury and reduced glomerular filtration rate (GFR), but in each case there must be an increase in arterial pressure to maintain salt and water balance.1–3 Thus, in long-standing diabetes, types 1 and 2, a progressive decline in GFR is matched by a reciprocal increase in arterial pressure, which enables maintenance of sodium balance and body fluid volume homeostasis at the expense of deleterious adverse effects of chronic hypertension.4

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 . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
T. D. Bell, G. F. DiBona, R. Biemiller, and M. W. Brands
Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked
Am J Physiol Renal Physiol, November 1, 2008; 295(5): F1449 - F1456.
[Abstract] [Full Text] [PDF]