Vol. 281, Issue 1, 434-439, 1997

Video-microscopic Assessment of the Role of Tissue Angiotensin-converting Enzyme in the Control of the Renal Microcirculation¹

P. M. Ter Wee², H. G. Forster and M. Epstein

Nephrology Section, Department of Veterans Affairs Medical Center, and Division of Nephrology, University of Miami School of Medicine, Miami, Florida

In the present study, we assessed the role of tissue angiotensin-converting enzyme as a determinant of intrarenal hemodynamics by using the angiotensin-converting enzyme inhibitor trandolaprilat and the angiotensin II receptor antagonist losartan. Afferent and efferent arteriolar diameters were measured with computer-assisted vessel imaging in isolated perfused hydronephrotic rat kidneys. In response to the addition of 1.0 nM angiotensin I, afferent arterioles constricted by 27.3 ± 2.4% and efferent arterioles by 20.9 ± 2.4%. These constrictions were similar to those observed after the administration of 0.3 nM angiotensin II (33.7 ± 2.3% and 20.9 ± 2.4% in afferent and efferent arterioles, respectively). Pretreatment with the angiotensin-converting enzyme inhibitor trandolaprilat (0.1-10 µM) blunted the angiotensin I-induced constriction of afferent arterioles (12.7 ± 1.4%) and completely abolished the angiotensin I-induced constriction of efferent arterioles. Subsequent addition of angiotensin II to the perfusate resulted in a marked decrease of afferent (39.9 ± 1.8%) and efferent (27.8 ± 3.3%) arteriolar diameters. Pretreatment with the angiotensin II receptor antagonist losartan completely blocked the angiotensin I-induced constriction of both afferent and efferent arterioles. Collectively, these data suggest that angiotensin I affects renal microvessels through its conversion to angiotensin II, mediated by locally available tissue angiotensin-converting enzyme, which subserves the local control of the renal microcirculation.