Increased tubuloglomerular feedback mediated suppression of GFR during acute volume expansion in rats
- JM Davis, DA Hiiberle, T Kawata, E Schmitt, T Takabatake, S Wohlfeil
- J Physiol (Lond)
Central to the assumption that glomerular capillary pressure (P gc) can be equated with the sum of arterial oncotic pressure (π art) and the pressure in a blocked proximal tubule (“stop flow” pressure, P sf) is that filtration ceases in the blocked nephron. Should filtration not cease, but continue at a rate equal to tubular reabsorption between the block and the glomerulus, P sf, for a given P gc, will depend on the distance between block and glomerulus. This would have serious consequences for the interpretation of P sf, particularly in respect of its frequent use in analysis of the tubuloglomerular feedback (TGF) mechanism. Experiments were performed in anaesthetized Wistar rats to examine whether a length dependency of P sf exists and, if so, to what extent this relationship alters during maximal TGF stimulation by loop of Henle perfusion. A length dependency of P sf existed both in the absence and presence of loop flow. The regression coefficients were significantly different from 0 and from each other. P gc cannot thus be equated with the sum of P sf and π art. The length dependent error in P sf makes it unsuitable for the quantitative analysis of TGF and glomerular haemodynamics.