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Neuronal nitric oxide synthase modulates rat renal microvascular function

A Ichihara1, E W Inscho, J D Imig

  • 1Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112-2699, USA.

The American Journal of Physiology
|April 8, 1998
PubMed
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Neuronal nitric oxide synthase (nNOS) influences kidney blood vessel tone based on fluid flow. nNOS enhances responses to angiotensin II in efferent but not afferent arterioles.

Area of Science:

  • Nephrology
  • Physiology
  • Vascular Biology

Background:

  • Neuronal nitric oxide synthase (nNOS) plays a role in regulating vascular tone.
  • The macula densa segment is crucial for tubuloglomerular feedback, influencing renal hemodynamics.
  • Angiotensin II (ANG II) is a key regulator of blood pressure and renal function.

Purpose of the Study:

  • To investigate the impact of nNOS on renal arteriolar tone under varying fluid delivery conditions.
  • To determine the influence of nNOS on microvascular responses to ANG II.
  • To elucidate the role of distal tubular fluid flow in mediating nNOS effects on renal arterioles.

Main Methods:

  • In vitro experiments using the blood-perfused juxtamedullary nephron technique in rat kidneys.
  • Utilized specific (S-methyl-L-thiocitrulline, L-SMTC) and nonselective (N omega-nitro-L-arginine, L-NNA) nNOS inhibitors.

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  • Manipulated distal volume delivery via papillectomy and acetazolamide administration.
  • Main Results:

    • Specific nNOS inhibition decreased afferent and efferent arteriolar diameters, an effect prevented by interrupting distal flow.
    • Increased macula densa flow enhanced afferent arteriolar constriction to nNOS inhibition, but this was abolished by papillectomy.
    • nNOS inhibition enhanced efferent, but not afferent, arteriolar vasoconstriction to ANG II, while nonselective inhibition affected both.

    Conclusions:

    • nNOS modulation of afferent arteriolar tone in juxtamedullary nephrons is dependent on distal tubular fluid flow.
    • nNOS differentially regulates the juxtamedullary microvasculature, enhancing efferent arteriolar responsiveness to ANG II.
    • These findings highlight the complex interplay between nNOS, fluid flow, and the renin-angiotensin system in renal hemodynamics.