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Am J Physiol Renal Physiol 276: F751-F757, 1999;
0363-6127/99 $5.00
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Vol. 276, Issue 5, F751-F757, May 1999

Tubuloglomerular feedback in ACE-deficient mice

Timothy Traynor1, Tianxin Yang1, Yuning G. Huang1, John H. Krege2,3, Josie P. Briggs1,4, Oliver Smithies2, and Jürgen Schnermann1

1 Departments of Physiology and Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109; 2 Department of Pathology, University of North Carolina, Chapel Hill, North Carolina 27599; 3 Guilford Medical Associates, Greensboro, North Carolina 27405; and 4 National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892

In these experiments, we used a strain of angiotensin converting enzyme (ACE) germline null mutant mice, generated by J. H. Krege and co-workers (J. H. Krege, S. W. M. John, L. L. Langenbach, J. B. Hodgin, J. R. Hagaman, E. S. Bachman, J. C. Jennette, D. A. O'Brien, and O. Smithies. Nature 375: 146-148, 1995), to examine the effect of chronic ACE deficiency on the magnitude of tubuloglomerular feedback (TGF) responses. The genotype was determined by PCR on DNA extracted from the tail and was verified after each experiment by assessment of the blood pressure response to an injection of ANG I. To assess TGF responsiveness, we determined the change in stop-flow pressure (PSF) caused by increasing NaCl concentration at the macula densa by using micropuncture techniques. When loop of Henle flow rate was increased from 0 to 40 nl/min, PSF fell from a mean of 42.3 ± 1.95 to 33.6 ± 2.09 mmHg (n = 6, P = 0.005) in wild-type mice (+/+), fell from 40.6 ± 2.35 to 38.6 ± 1.93 mmHg in heterozygous (+/-) mice (n = 7, P = 0.014), and did not change in homozygous ACE (-/-) mice [36.7 ± 2.02 mmHg vs. 36.4 ± 2.01 mmHg; n = 4, P = not significant (NS)]. During an infusion of ANG II at a dose that did not significantly elevate blood pressure (70 ng · kg-1 · min-1), TGF response magnitude (PSF 0 - PSF 40) increased from 6.5 ± 1.4 to 9.8 ± 1.19 mmHg in +/+ (P = 0.006), from 1.14 ± 0.42 to 4.6 ± 1.3 mmHg in +/- (P = 0.016), and from 0.42 ± 0.25 to 4.02 ± 1.06 in -/- mice (P = 0.05). Absence of TGF responses in ACE null mutant mice and restoration of near-normal responses during an acute infusion of ANG II supports previous conclusions that ANG II is an essential component in the signal transmission pathway that links the macula densa with the glomerular vascular pole.

transgenic mouse; gene knockout; micropuncture; angiotensin converting enzyme; stop-flow pressure


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