What question did this study set out to answer?

To examine the role of the nitric oxide pathway in controlling renal vascular tone and renin secretion under differing levels of dietary salt intake.

November 1, 1994AJP Renal Physiology

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction

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Why the study?

Does L-NAME affect renin release and renal vasoconstriction differently in isolated kidneys from rats on low versus high sodium diets?

Population

Isolated perfused rat kidney model from rats exposed to low or high salt intake for 1 month

Comparison

NG-nitro-L-arginine methyl ester 1-25 microM vs Comparison between low salt and high salt intake…

Design

Preclinical

Follow-up

1 month (duration of salt diet exposure)

Authors

JGJ. GardesDélégation Paris 5 MGM. F. GonzalezInstitut National de Santé Publique FAFrançois Alhenc‐GelasInserm

Discussion

Member takes

Implication

Supports NO counter-regulation of high-salt renal vasoconstriction in rats; leaves open translation to human salt sensitivity or hypertension.

Key Points

To examine the role of the nitric oxide pathway in controlling renal vascular tone and renin secretion under differing levels of dietary salt intake.
Perfused isolated rat kidneys with the nitric oxide synthase inhibitor L-NAME (1–25 µM) under constant or variable perfusion pressure.
Maintained rats on either a low-salt (salt-depleted) or high-salt (salt-repleted) diet for one month before assessing renal vascular and renin responses to 3 µM L-NAME.
L-NAME produced a dose-dependent increase in perfusion pressure, a decrease in perfusate flow, and an inhibition of renin release that occurred independently of pressure changes.
Kidneys from salt-repleted rats displayed significantly greater vasoconstriction in response to L-NAME than kidneys from salt-depleted rats.
L-NAME provoked a similar absolute reduction in renin secretion in both dietary groups, despite salt-depleted rats having higher baseline renin output.

Structured PICO

Does L-NAME affect renin release and renal vasoconstriction differently in isolated kidneys from rats on low versus high sodium diets?

Population

Isolated perfused rat kidney model from rats exposed to low (salt depleted, SD) or high (salt repleted, SR) salt intake for 1 month

Intervention

NG-nitro-L-arginine methyl ester (L-NAME) 1-25 microM (specifically 3 microM for salt diet comparison)

Comparator

Comparison between low salt (SD) and high salt (SR) intake groups, and baseline without L-NAME

Outcome

Renal vasodilation (perfusion pressure and renal perfusate flow) and renin secretion/releasesurrogate

In a rat model, NO-dependent vasodilation appears to counteract the renal vasoconstrictor effect of sodium loading, with high salt intake enhancing the vasoconstrictive response to NO synthase inhibition.

Cite This Study

Gardes et al. (1994) studied this question.

synapsesocial.com/papers/6a83fa94b0b8dfdc4c62e76f https://doi.org/10.1152/ajprenal.1994.267.5.f798

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Implication

Supports NO counter-regulation of high-salt renal vasoconstriction in rats; leaves open translation to human salt sensitivity or hypertension.

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider