Resetting of tubuloglomerular feedback by interrupting early distal flow.

Cell-cell contact between the macula densa and the glomerular arterioles is is thought to provide the information pathway for the tubuloglomerular feedback (TGF) mechanism. When concentrations of sodium and chloride in the macula densa segment are increased, a signal is transmitted through the extraglomerular mesangium to contract the afferent arteriole. In addition, some observers have described a second region of contact between a later part of the distal tubule and the afferent arteriole of the same nephron. In this region the connecting tubule (CNT), and sometimes nerves that make contact with the cells of this CNT, were found. This arrangement gives another potential tubular segment, besides the macula densa plaque, in which the composition of tubular fluid may regulate glomerular dynamics. The present study was designed to investigate whether interrupting flow in the distal tubule downstream from the macula densa would influence the TGF mechanism. TGF was examined in rats by orthograde microperfusion, before and after blockade of the distal nephron with castor oil. Two variables were measured: maximum decrease in stop-flow pressure (delta Psf), and perfusion rate which elicits half-maximal decrease in delta Psf (V1/2). The fluid arriving at the blocking point was collected into a micro-pipette. The results show a significant increase in V1/2 from 19 to 25 nl min-1 after 30 min of blockade. In conclusion the results support a role of the distal nephron in the control of the TGF mechanism.