Maintenance of feedback regulation of filtration dynamics in the absence of divalent cations in the lumen of the distal tubule.

In the present experiments we have studied the hypothesis that the feedback responses of glomerular capillary pressure and glomerular filtration rate to elevated distal fluid delivery depend to some extent on the luminal concentration of calcium or magnesium [1]. Loops of Henle were therefore perfused with the following solutions which were designed to yield wide variations of distal divalent cation concentration: 1. Ringer, 2. 140mM NaCl, 3. 125mM NaCl + 10mM CaCl2, 4. 125 mM NaCl + 10 mM MgCl2, 5. 125 mM NaCl + 10 mM Na citrate, and 6. 125 mM NaCl + 10 mM EDTA. During orthograde perfusion with these solutions stop flow pressure (SEP) and early proximal flow rate (EPFR) were measured in each nephron at perfusion rates of 0, 15, 30, and 45 nl/min. We found that perfusion with solutions 2 to 6 did not significantly modify the flow induced change of SFP or EPFR observed during Ringer perfusion. To expose the macula densa cells to chemically well defined solutions loops of Henle were retrogradely perfused from the distal tubule and EPFR was measured in a given nephron with and without perfusion. Identical reductions of EPFR were induced by retrograde perfusions with 140 mM NaCl, 125 mM NaCl + 10 mM CaCl2, and 125 mM NaCl + 10 mM EDTA. Furthermore, an almost complete blunting of the feedback response was noted during retrograde perfusion with 25 mM NaCl. Addition of 5 mM CaCl2 failed to restore the feedback reaction. These results do not support the concept that luminal divalent cations participate in the initiation of tubulo-glomerular feedback responses.