Effects of barium ions on tubuloglomerular feedback.
Schnermann, Jurgen.
Department of Physiology, The University of Michigan, Ann Arbor,
Michigan 48104
APStracts 2:0009F, 1995.
The furosemide sensitivity of the tubuloglomerular feedback response
has suggested an important role for the Na,2Cl,K-cotransporter in the
mechanism by which increased luminal NaCl concentration causes
afferent arteriolar vasoconstriction. The present experiments in
anesthetized rats were done to evaluate the effect of potassium
channel blockade with barium on tubuloglomerular feedback since
barium has been shown to inhibit NaCl transport in the thick
ascending limb. The presence of either 1.5 or 2 mM BaCl2 during
retrograde perfusion with a 135 mM NaCl solution reduced the decrease
of early proximal flow rate (VEP) by 2.7 +/- 0.76 nl/min (p < 0.02) and
4.2 +/- 0.8 nl/min (p < 0.01) compared to perfusion without BaCl2.
Retrograde perfusion with 38 mM NaCl plus 5 mM KCl reduced VEP by
10.4 +/- 1.3 nl/min whereas 40 mM NaCl plus 1.5 mM BaCl2 caused a
reduction by only 6.1 +/- 1.4 nl/min (p < 0.001). In contrast to the
inhibition caused by retrograde perfusion with low concentrations of
BaCl2, increased vasoconstriction was seen during retrograde
perfusion with 5 mM BaCl2, or during orthograde perfusion with 10 mM
BaCl2. The addition of 10-4 M furosemide to a solution containing 5
mM BaCl2 largely blocked the increased vasoconstrictor response.
Peritubular perfusion with a solution containing 5 mM BaCl2 caused a
fall in stop flow pressure in an adjacent nephron by 10.7 +/- 1.5 mm Hg
(p < 0.001). These results indicate that under our experimental
conditions barium ions exert a dual effect on vascular responses to
changes in luminal NaCl concentration. At low concentrations of
barium TGF responses were significantly reduced supporting the notion
that NaCl transport rate is a component of the signalling pathway.
However, at higher concentrations of barium TGF responses were
augmented, presumably by a direct vasoconstrictor effect of barium.
Received 7 October 1994; accepted in final form 23 December 1994.
APS Manuscript Number F357-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.