AJP - Renal Physiology, Vol 260, Issue 4 486-F493, Copyright © 1991 by American Physiological Society
Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport
J. N. Lorenz, H. Weihprecht, J. Schnermann, O. Skott and J. P. Briggs
Department of Physiology, University of Michigan, Ann Arbor 48109.
Transport inhibitor and ion substitution studies were performed using
perfused, superfused preparations of the isolated rabbit juxtaglomerular
apparatus to investigate transport dependency of macula densa-mediated
renin secretion. In the first experimental series, tubular perfusion with a
high-NaCl solution containing 10(-6) M bumetanide increased renin secretion
compared with perfusion with high NaCl alone from 8.7 to 24.6
nano-Goldblatt hog units (nGU)/min. Bath addition of 10(-6) M bumetanide
had no effect on renin release. The second series tested ability of luminal
addition of 54 mmol/l Na or Cl salts to inhibit renin secretion, starting
from a stimulated value produced by low-NaCl perfusion. Perfusion with a
high-NaCl solution decreased renin secretion from 58.9 to 14.8 nGU/min,
which served as a positive control. Addition of choline chloride decreased
renin secretion from 42.7 to 16.6 nGU/min, and RbCl decreased renin
secretion from 54.9 to 17.0 nGU/min. In contrast, addition of two different
Na salts had no effect on renin release (from 41.7 to 31.6 nGU/min with
sodium isethionate and from 14.1 to 13.5 nGU/min with sodium acetate).
Also, in the presence of 26 mmol/l Cl, addition of 54 mmol/l Na had no
effect on renin secretion (29.9-36.8 nGU/min). These data demonstrate that
renin secretion is directly stimulated by luminal application of transport
blockers and can be inhibited by increases in Cl concentration at the
macula densa but not by changes in Na concentration. These results support
the hypothesis that the initiating signal for macula densa control of renin
secretion is an inverse change in transport rate via the luminal
Na(+)-K(+)-2Cl- cotransporter.
