Increased tubular flow induces resetting of tubuloglomerular
feedback in euvolemic rats.
Thomson, Scott C., Roland C. Blantz, and Volker Vallon.
Department of Medicine, Division of Nephrology/Hypertension, Univ.
of California and Veterans Affairs Medical Center, San Diego, CA
APStracts 2:0178F, 1995.
As nephron GFR (SNGFR) and late proximal flow (VLP) increase during
growth or following volume expansion, the TGF function (defined as
the decrement in SNGFR due to the process of tubuloglomerular
feedback) shifts rightward in the plane defined by VLP and SNGFR as
is required to maintain the homeostatic efficiency of TGF. It is not
known whether this resetting of TGF requires changes in the systemic
hormonal milieu or results from prolonged activation of TGF itself.
We employed micropuncture and videometric flow velocitometry (an
optical technique for measuring flow in unobstructed nephrons) to
address this issue in Inactin-anesthetized euvolemic rats. The
fractional compensation (C) of TGF for perturbations (VH=+/-5 nl/min)
in VLP was assessed repeatedly, before and during a sustained
increase in flow imposed by adding 20 nl/min to early proximal flow
(VEP). Augmenting VEP initially saturated TGF, thus suppressing C.
Over the next 30 minutes C recovered to 70% of its original value,
suggesting a rightward resetting of the TGF function to match the
increase imposed on VLP. Resetting was confirmed by documenting an
evolving asymmetry of C about VH=0 by testing C vs. VH for
-12=VH=12 in increments of 4 nl/min. Beyond 30 minutes of
augmented VEP, C gradually declined due to desensitization of TGF. A
sustained increase in VLP is sufficient to induce TGF resetting
independent of any change in the systemic neurohumoral milieu.
Received 3 April 1995; accepted in final form 19 September 1995.
APS Manuscript Number F113-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95