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Converting Enzyme Inhibition and the Glomerular Hemodynamic Response to Glycine in Diabetic Rats

LARRY A. SLOMOWITZ^*, ORJAN W. PETERSON and SCOTT C. THOMSON

^* Baylor School of Medicine, Houston, Texas
Department of Medicine, Division of Nephrology/Hypertension, Veterans Affairs Medical Center and University of California, San Diego, California.

Correspondence to Dr. Scott C. Thomson, Associate Professor of Medicine, Division of Nephrology/Hypertension, University of California, San Diego, and San Diego Veterans Affairs Medical Center, 3350 La Jolla Village Drive, San Diego, CA 92161-9151. Phone: 619-552-8585, ext. 3793; Fax: 619-552-7549; E-mail: sthomson{at}ucsd.edu

Abstract. GFR normally increases during glycine infusion. This response is absent in humans and rats with established diabetes mellitus. In diabetic patients, angiotensin-converting enzyme inhibition (ACEI) restores the effect of glycine on GFR. To ascertain the glomerular hemodynamic basis for this effect of ACEI, micropuncture studies were performed in male Wistar-Froemter rats after 5 to 6 wk of insulin-treated streptozotocin diabetes. The determinants of single-nephron GFR (SNGFR) were assessed in each rat before and during glycine infusion. Studies were performed in diabetics, diabetics after 5 d of ACEI (enlapril in the drinking water), and weight-matched controls. Diabetic rats manifest renal hypertrophy and glomerular hyperfiltration but not glomerular capillary hypertension. ACEI reduced glomerular capillary pressure, increased glomerular ultrafiltration coefficient, and did not mitigate hyperfiltration. In controls, glycine increased SNGFR by 30% due to increased nephron plasma flow. In diabetics, glycine had no effect on any determinant of SNGFR. In ACEI-treated diabetics, the SNGFR response to glycine was indistinguishable from nondiabetics, but the effect of glycine was mediated by greater ultrafiltration pressure rather than by greater plasma flow. These findings demonstrate that: (1) The absent response to glycine in established diabetes does not indicate that renal functional reserve is exhausted by hyperfiltration; and (2) ACEI restores the GFR response to glycine in established diabetes, but this response is mediated by increased ultrafiltration pressure rather than by increased nephron plasma flow.

This article has been cited by other articles:

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