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Related Experiment Videos

Macula densa nitric oxide synthase: expression, regulation, and function

C S Wilcox1, W J Welch

  • 1Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington, DC 20007, USA. wilcoxch@gunet.georgetown.edu

Kidney International. Supplement
|September 15, 1998
PubMed
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Dietary salt restriction limits nitric oxide (NO) generation in kidney macula densa cells due to reduced L-arginine availability, despite increased brain nitric oxide synthase (bNOS) expression. This impacts renal adaptation mechanisms.

Area of Science:

  • Nephrology
  • Renal Physiology
  • Molecular Biology

Background:

  • Type 1 brain nitric oxide synthase (bNOS) in macula densa (MD) cells regulates afferent arteriole vasodilation and tubuloglomerular feedback (TGF).
  • Dietary salt restriction increases bNOS expression, but its functional activity in MD cells remains unclear.
  • Limited L-arginine (L-Arg) availability may impair NO generation in MD cells during low salt intake.

Purpose of the Study:

  • To investigate the hypothesis that reduced L-arginine availability limits MD NO generation during low salt intake.
  • To elucidate the mechanism by which salt restriction affects NO-mediated TGF regulation in the kidney.

Main Methods:

  • Maximal TGF responses were measured during Henle's loop perfusion with artificial tubular fluid (ATF) in rats on varying salt diets.

Related Experiment Videos

  • L-arginine was microperfused into the MD of low-salt (LS) rats to assess its effect on TGF.
  • Stereospecificity, inhibition by monomethyL-L-arginine (L-NMA), and dependence on system y+ transport for L-Arg response were evaluated.
  • Absorption of [3H]-L-Arg from the perfused loop was measured under different salt conditions.

    • Main Results:

    • Microperfusion of L-Arg into the MD blunted maximal TGF responses in LS rats, but not in normal or high-salt (HS) rats.
    • The L-Arg effect was stereospecific, inhibited by L-NMA, and dependent on system y+ transport, as shown by blockade with L-lysine or L-homoarginine.
    • L-Arg absorption from the perfused loop was enhanced during HS via an L-Arg- or L-homoarginine-inhibitable process.

    Conclusions:

    • Salt restriction diminishes NO-mediated TGF attenuation in the MD despite increased bNOS expression.
    • This occurs due to limited delivery and/or uptake of L-arginine via system y+.
    • This defines a novel mechanism of renal microcirculatory adaptation to salt restriction involving L-arginine-dependent changes in TGF.