Document Detail


Impaired renal blood flow and cortical pressure autoregulation in contralateral kidneys of Goldblatt hypertensive rats.
MedLine Citation:
PMID:  7203607     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Experiments were conducted on two-kidney, one clip renal vascular hypertensive rats to assess the ability of the kidney contralateral to renal vascular stenosis to autoregulate renal blood flow (RBF), glomerular filtration rate (GFR), and hydrostatic pressures in cortical structures during conditions of acutely reduced renal arterial blood pressure (BP). When observed at their respective, spontaneous BPs, RBF and GFR were not different in the contralateral kidneys of the hypertensive rats (n = 11) compared to normal animals (n = 7). However, the contralateral kidneys exhibited a significantly higher renal vascular resistance (RVR), 28.9 +/- 2.8 mm Hg . min/ml than the control animals, 23.1 +/- 1.5 mm Hg . min/ml. At spontaneous BP (169 +/- 5 mm Hg), urine flow, absolute and fractional sodium excretion, and absolute and fractional potassium excretion were all significantly greater in the contralateral kidneys of hypertensive rats than in kidneys of normal rats. Hydrostatic pressures in cortical structures were similar in the two groups. When BP was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in RVR that failed to allow RBF, GFR, or cortical pressures to be maintained. In contrast, normal rats efficiently autoregulated RBF and GFR. In addition, hydrostatic pressures in proximal tubules, distal tubules, and first order peritubular capillaries were maintained during reductions in BP to as low as 100 mm Hg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys, such that at comparable BP these indices of excretory function were not different in the two groups. These observations indicate that the capacity of the contralateral kidney to maintain hemodynamic and glomerular function at reduced BP is compromised severely and suggest the possibility that the impaired autoregulatory capability may contribute to the maintenance of hypertension observed in this model.
Authors:
D W Ploth; R N Roy; W C Huang; L G Navar
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Hypertension     Volume:  3     ISSN:  0194-911X     ISO Abbreviation:  Hypertension     Publication Date:    1981 Jan-Feb
Date Detail:
Created Date:  1981-05-13     Completed Date:  1981-05-13     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  67-74     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure
Glomerular Filtration Rate
Hydrostatic Pressure
Hypertension, Renal / physiopathology*
Hypertension, Renovascular / physiopathology*
Kidney / blood supply*,  metabolism
Kidney Cortex / physiopathology*
Potassium / urine
Rats
Regional Blood Flow
Renal Artery Obstruction / physiopathology
Sodium / urine
Urodynamics
Vascular Resistance
Chemical
Reg. No./Substance:
7440-09-7/Potassium; 7440-23-5/Sodium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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