Tubuloglomerular feedback dependence of autoregulation in rat juxtamedullary afferent arterioles

LC Moore, D Casellas - Kidney international, 1990 - Elsevier
LC Moore, D Casellas
Kidney international, 1990Elsevier
Tubuloglomerular feedback dependence of autoregulation in rat juxta-medullary afferent
arterioles. Experiments were performed in blood-perfused juxtamedullary nephrons in vitro
to evaluate the tubuloglomerular feedback (TGF) dependence of autoregulatory
vasoconstriction in mid-to-late (mAA) and juxtaglomerular (jAA) afferent arterioles. Video-
metric measurements were made of perfusion pressure (PP) dependent changes in lumen
diameter of superficial vessels before and after acute inhibition of the TGF mechanism by …
Tubuloglomerular feedback dependence of autoregulation in rat juxta-medullary afferent arterioles. Experiments were performed in blood-perfused juxtamedullary nephrons in vitro to evaluate the tubuloglomerular feedback (TGF) dependence of autoregulatory vasoconstriction in mid-to-late (mAA) and juxtaglomerular (jAA) afferent arterioles. Video-metric measurements were made of perfusion pressure (PP) dependent changes in lumen diameter of superficial vessels before and after acute inhibition of the TGF mechanism by direct microinfusion of 0.1 mM furosemide solution into the macula densa (MD) segment. When PP was raised from 60 to 123 ± 7 mm Hg in seven vessels, jAA diameter decreased by 29 ± 3% (SEM, N = 7). During furosemide infusion with the same change in PP, jAA diameter decreased only 7 ± 2%. After calcium channel blockade with 1 micromolar nimodipine, jAA lumen diameter increased by 21 ± 7%. A similar pattern of responses was observed in eight jAA where TGF was inhibited with an oil block at the MD. mAA autoregulatory responses were also blunted by TGF inhibition. Raising PP from 60 to 120 mm Hg resulted in 15 ± 2% and 7 ± 2% decreases in mAA luminal diameter before and after TGF inhibition. These results demonstrate that the autoregulatory responses in mid- and juxtaglomerular afferent arteriolar segments are mediated by both TGF and a TGF-independent myogenic mechanism.
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