F. JUNG, AND JULIE R. INGELFINGER (With the Technical Assistance of Boutros Bouyounes, Julia L. Troy, and Miguel A. Zayas) Renal Division, Department of Medicine, Brigham and Womenâs Hospital, Boston 02115; Division of Pediatric Nephrology, Massachusetts General Hospital, Boston, Massachusetts 02114 Anderson, Sharon, Flavia F. Jung, and Julie R. Ingelfinger. Renal in diabetes:functional, Am. J. Physiol. 265 (Renal Fluid Electrolyte immunohistochemical, and molecular biological correlations. Physiol. 34): F477F486, 1993.-Recent evidence indicates a role for the reninangiotensin (RAS) in the pathogenesisof glomerular injury in diabetes. To further explore the RAS in diabetes, studieswere conducted in nondiabetic control and in moderately hyperglycemic diabetic () . In , both acute and chronic therapy with the specific angiotensin II (ANG II) receptor antagonist losartan did not affect glomerular hyperfiltration or hyperperfusion but selectively normalized the glomerularcapillary hydraulic pressureand ultrafiltration coefficient. To determine the basisof intrarenal hemodynamic responsiveness RAS inhibition, we conductedbiochemical,moto lecular biological, and immunohistochemicalstudies to assess endogenous RAS activity. Values for plasmarenin concentration and serumangiotensin-converting enzyme (ACE) activity in were normal. In contrast, intrarenal renin protein content, and renin and angiotensinogen mRNAs, were increasedin , suggestingdisproportionate activation of the intrarenal RAS. Total renal ACE activity wassignificany reduced in , but immunohistochemical
AJP - Renal Physiology – The American Physiological Society
Published: Oct 1, 1993
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