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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/F1324    most recent 90363.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Yingst, D. R. Articles by Beierwaltes, W. H. PubMed PubMed Citation Articles by Yingst, D. R. Articles by Beierwaltes, W. H.

Decreased renal perfusion rapidly increases plasma membrane Na-K-ATPase in rat cortex by an angiotensin II-dependent mechanism

¹Department of Physiology, ; ²Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, and ; ³Department of Pharmacology, Wayne State University School of Medicine, Detroit; and ; ⁴Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan

Submitted June 11, 2008 ; accepted in final form August 27, 2009

To understand how rapid changes in blood pressure can regulate Na-K-ATPase in the kidney cortex, we tested the hypothesis that a short-term (5 min) decrease in renal perfusion pressure will increase the amount of Na-K-ATPase in the plasma membranes by an angiotensin II-dependent mechanism. The abdominal aorta of anesthetized Sprague-Dawley rats was constricted with a ligature between the renal arteries, and pressure was monitored on either side during acute constriction. Left renal perfusion pressure was reduced to 70 ± 1 mmHg (n = 6), whereas right renal perfusion pressure was 112 ± 4 mmHg. In control (nonconstricted) rats (n = 5), pressure to both kidneys was similar at 119 ± 6 mmHg. After 5 min of reduced perfusion, femoral venous samples were taken for plasma renin activity (PRA) and the kidneys excised. The cortex was dissected, minced, sieved, and biotinylated. Lower perfusion left kidneys showed a 41% increase (P < 0.003) in the amount of Na-K-ATPase in the plasma membrane compared with right kidneys. In controls, there was no difference in cell surface Na-K-ATPase between left and right kidneys (P = 0.47). PRA was 57% higher in experimental animals compared with controls. To test the role of angiotensin II in mediating the increase in Na-K-ATPase, we repeated the experiments (n = 6) in rats treated with ramiprilat. When angiotensin-converting enzyme was inhibited, the cell surface Na-K-ATPase of the two kidneys was equal (P =0.46). These results confirm our hypothesis: rapid changes in blood pressure regulate trafficking of Na-K-ATPase in the kidney cortex.

ouabain; sodium; blood pressure; renin