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Am J Physiol Renal Physiol (October 19, 2004). doi:10.1152/ajprenal.00297.2004
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Submitted on August 10, 2004
Accepted on October 9, 2004

Micropuncture determination of nephron function in mice without tissue angiotensin converting enzyme

Seiji Hashimoto1, Jon W. Adams2, Kenneth E. Bernstein2, and Jurgen Schnermann1*

1 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
2 Department of Pathology, Emory University, Atlanta, GA, USA

* To whom correspondence should be addressed. E-mail: jurgens{at}intra.niddk.nih.gov.

To determine the role of the local renin-angiotensin system on renal function, micropuncture was performed on two lines of mice in which genetic changes to the ACE gene markedly reduced or eliminated the expression of renal tissue ACE. Whereas blood pressure is low in one line (ACE 2/2), it is normal in the other (ACE 1/3) due to ectopic hepatic ACE expression. When normalized for renal size, levels of GFR (µl/min.g KW) and SNGFR (nl/min.g KW) were similar between wild-type (WT) and ACE 1/3 mice, while both measures were significantly reduced in AC E 2/2 mice (WT: 500 ± 63 and 41.7 ± 3.5; ACE 1/3: 515.8 ± 71 and 44.3 ± 3.3; ACE 2/2: 131.4 ± 23 and 30.3 ± 3.5). Proximal fractional reabsorption was not significantly different between WT, and ACE 1/3 mice (51 ± 3.5 %, and 49 ± 2.3 %), and it was increased significantly in ACE 2/2 mice (74 ± 3.5%). Infusion of angiotensin II (50 ng/kg min) increased mean arterial pressure by about 7 mm Hg in all groups of mice, and reduced SNGFR in WT and ACE 1/3 mice (to 30.9 ± 2.8, and 31.9 ± 2.5 nl/min.g KW), while increasing SNGFR in ACE 2/2 mice (to 55.3 ± 5.3 nl/min.g KW) despite an increase in total renal vascular resistance. Tubuloglomerular feedback (TGF) response was markedly reduced in ACE 1/3 mice (PSF change -2.5 ± 0.9 mm Hg) as compared to WT despite similar blood pressures (-8.3 ± 0.6 mm Hg). In ACE 2/2 mice, TGF was absent (-0.7 ± 0.2 mm Hg). We conclude that the chronic lack of ACE, and presumably angiotensin II generation, in the proximal tubule was not associated with sustained proximal fluid transport defects. However, renal tissue ACE is an important contributor to tubuloglomerular feedback.




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