Glomerular and renal hemodynamics during converting enzyme inhibition (SQ20,881) in the dog

Academic Article

Abstract

  • It has been suggested that intrarenal levels of angiotensin II may preferentially control efferent arterlolar resistance or may influence the glomerular filtration coefficient (KT). To examine these possibilities, micropuncture and clearance experiments were performed on nine anesthetized dogs evaluating renal and glomerular hemodynamics before and during the administration of an angiotensin converting enzyme inhibitor (SQ20,881). During the micropuncture measurements, renal arterial pressure was reduced to a range of 85 to 90 mm Hg in order to maximize renin secretion and intrarenal formation of angiotensin II. Also, this procedure minimizes potential errors In the determination of single nephron glomerular filtration rate (SNGFR) and of glomerular pressure when estimated by techniques that require complete blockade of proximal tubule fluid flow. During the administration of SQ20,881, a converting enzyme inhibitor (CEI), renal blood flow increased significantly by 13%, but GFR was not altered. There were no significant alterations in SNGFR, proximal tubule pressure, peritubular capillary pressure or estimated glomerular pressure. By using the micropressure measurements in combination with the whole kidney hemodynamic data, it was estimated that afferent resistance was reduced 23%. Although significant decreases in efferent resistance could not be documented, there was a tendency for this variable to decrease also. Neither Kr nor effective filtration pressure were altered significantly by CEI. These results do not support the contention that intrarenal effects of angiotensin II are exerted predominantly on the efferent arteriolar resistance segments; rather, they suggest that angiotensin may exert a modest tonic effect on both pre-and postglomeralar resistance elements in the anesthetized hydropenic dog. © 1979 American Heart Association, Inc.
  • Authors

    Author List

  • Gabriel Navar L; Lagrange RA; Bell PD; Thomas CE; Ploth DW
  • Start Page

  • 371
  • End Page

  • 377
  • Volume

  • 1
  • Issue

  • 4