Importance of Efferent Arteriolar Vascular Tone in Regulation of Proximal Tubule Fluid Reabsorption and Glomerulotubular Balance in the Rat

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Abstract

Micropuncture study was performed in 21 mildly volume-expanded Munich-Wistar rats before and during partial aortic constriction to examine the effects of endogenous prostaglandins (PG) and angiotensin II (AII) on single nephron glomerular filtration rate (SNGFR) and absolute proximal reabsorption rate (APR). Animals received either vehicle (group 1), indomethacin (group 2), or indomethacin plus saralasin (group 3). Before aortic constriction, these inhibitors were without effect on values of SNGFR and APR. In group 1 rats, reduction in mean renal arterial perfusion pressure (R̄ĀP̄) to ∼65 mm Hg resulted in marked and proportional declines in SNGFR and APR. With equivalent reduction in R̄ĀP̄ in group 2 rats, however, SNGFR fell to a lesser extent and APR tended to increase slightly above preconstriction values. Indomethacin administration was therefore associated with disruption of glomerulotubular balance. In view of the roughly equivalent declines in afferent arteriolar resistance measured in groups 1 and 2, the magnitude of increase in efferent arteriolar resistance (RE) appeared to be of major importance in determining the observed presence or absence of glomerulotubular balance. Thus, the lesser fall in SNGFR in group 2 than in group 1 was a result of the higher value for glomerular capillary hydraulic pressure in group 2, a consequence of the higher value of RE. The higher average value for APR during reduced R̄ĀP̄ in group 2 than in group 1 is also attributable to this pronounced rise in RE, the effect of which was to augment the net reabsorptive pressure both by favoring higher postglomerular oncotic pressure and lower downstream (peritubular capillary) hydraulic pressure. Since intrarenal release of AII is enhanced when R̄ĀP̄ declines, and because AII is known to raise RE selectively, it is likely that endogenous AII brought about the marked increase in RE in group 2, which was readily demonstrable only in indomethacin-treated rats, presumably because endogenous PG synthesis was suppressed.

Authors

Iekuni Ichikawa, Barry M. Brenner