What question did this study set out to answer?

To determine whether basal presence of nitric oxide or dynamic alterations in its production are required to mediate renal pressure natriuresis.

October 1, 1993Hypertension

Renal responses to intra-arterial administration of nitric oxide donor in dogs.

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Why the study?

Does intra-arterial administration of a nitric oxide donor (SNAP) restore pressure natriuresis and renal blood flow in dogs treated with a nitric oxide synthesis inhibitor (NLA)?

Population

Anesthetized sodium-replete dogs (n = 8)

Comparison

Intra-arterial infusion of… vs Baseline and NLA infusion alone

Design

Preclinical

Authors

DMDewan S. A. MajidTulane University AWAleck F. WilliamsMidlands Technical College PKPhilip J. KadowitzMarquette University

Discussion

Member takes

Implication

Supports nitric oxide modulation of renal function in experimental models; leaves open translation to human hypertension.

Key Points

To determine whether basal presence of nitric oxide or dynamic alterations in its production are required to mediate renal pressure natriuresis.
Assessed anesthetized, sodium-replete dogs (n = 8) receiving intra-arterial nitro-L-arginine (50 µg·kg⁻¹·min⁻¹) to inhibit endogenous nitric oxide synthesis.
Infused the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP; 2 µg·kg⁻¹·min⁻¹) intra-arterially at a constant rate to restore intrarenal nitric oxide during reductions in renal arterial pressure.
Nitro-L-arginine alone increased renal vascular resistance and decreased renal blood flow, urine flow, and sodium excretion while preserving autoregulatory efficiency and attenuating pressure-induced natriuresis.
Coadministration of SNAP increased renal blood flow from 2.8 ± 0.3 to 3.5 ± 0.3 mL·min⁻¹·g⁻¹ (P < .001) without significantly altering glomerular filtration rate (0.75 ± 0.07 to 0.81 ± 0.05 mL·min⁻¹·g⁻¹).
SNAP administration elevated urine flow (4.8 ± 1.8 to 10.0 ± 2.5 µL·min⁻¹·g⁻¹), sodium excretion (0.63 ± 0.26 to 1.70 ± 0.37 µmol·min⁻¹·g⁻¹), and fractional excretion of sodium (0.55 ± 0.20% to 1.38 ± 0.27%).

Structured PICO

Does intra-arterial administration of a nitric oxide donor (SNAP) restore pressure natriuresis and renal blood flow in dogs treated with a nitric oxide synthesis inhibitor (NLA)?

Population

Anesthetized sodium-replete dogs (n = 8)

Intervention

Intra-arterial infusion of S-nitroso-n-acetylpenicillamine (SNAP) at a constant rate (2 micrograms.kg-1 x min-1) during nitro-L-arginine (NLA) infusion (50 micrograms.kg-1 x min-1)

Comparator

Baseline and NLA infusion alone

Outcome

Renal responses to reductions in renal arterial pressure (RAP) including renal blood flow, glomerular filtration rate, urine flow, sodium excretion, and fractional excretion of sodiumsurrogate

Intra-arterial administration of a nitric oxide donor restores renal blood flow and sodium excretion in dogs with inhibited endogenous nitric oxide synthesis.

Cite This Study

Majid et al. (1993) studied this question.

synapsesocial.com/papers/6a87367ce0e6abca40d3cbc1 https://doi.org/10.1161/01.hyp.22.4.535

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October 1, 1993Hypertension

Renal responses to intra-arterial administration of nitric oxide donor in dogs.

View Full Paper

Ask AI

Bookmark

Why the study?

Does intra-arterial administration of a nitric oxide donor (SNAP) restore pressure natriuresis and renal blood flow in dogs treated with a nitric oxide synthesis inhibitor (NLA)?

Population

Anesthetized sodium-replete dogs (n = 8)

Comparison

Intra-arterial infusion of… vs Baseline and NLA infusion alone

Design

Preclinical

Authors

DMDewan S. A. MajidTulane University AWAleck F. WilliamsMidlands Technical College PKPhilip J. KadowitzMarquette University

Discussion

Member takes

Implication

Supports nitric oxide modulation of renal function in experimental models; leaves open translation to human hypertension.

Key Points

To determine whether basal presence of nitric oxide or dynamic alterations in its production are required to mediate renal pressure natriuresis.
Assessed anesthetized, sodium-replete dogs (n = 8) receiving intra-arterial nitro-L-arginine (50 µg·kg⁻¹·min⁻¹) to inhibit endogenous nitric oxide synthesis.
Infused the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP; 2 µg·kg⁻¹·min⁻¹) intra-arterially at a constant rate to restore intrarenal nitric oxide during reductions in renal arterial pressure.
Nitro-L-arginine alone increased renal vascular resistance and decreased renal blood flow, urine flow, and sodium excretion while preserving autoregulatory efficiency and attenuating pressure-induced natriuresis.
Coadministration of SNAP increased renal blood flow from 2.8 ± 0.3 to 3.5 ± 0.3 mL·min⁻¹·g⁻¹ (P < .001) without significantly altering glomerular filtration rate (0.75 ± 0.07 to 0.81 ± 0.05 mL·min⁻¹·g⁻¹).
SNAP administration elevated urine flow (4.8 ± 1.8 to 10.0 ± 2.5 µL·min⁻¹·g⁻¹), sodium excretion (0.63 ± 0.26 to 1.70 ± 0.37 µmol·min⁻¹·g⁻¹), and fractional excretion of sodium (0.55 ± 0.20% to 1.38 ± 0.27%).

Structured PICO

Does intra-arterial administration of a nitric oxide donor (SNAP) restore pressure natriuresis and renal blood flow in dogs treated with a nitric oxide synthesis inhibitor (NLA)?

Population

Anesthetized sodium-replete dogs (n = 8)

Intervention

Intra-arterial infusion of S-nitroso-n-acetylpenicillamine (SNAP) at a constant rate (2 micrograms.kg-1 x min-1) during nitro-L-arginine (NLA) infusion (50 micrograms.kg-1 x min-1)

Comparator

Baseline and NLA infusion alone

Outcome

Renal responses to reductions in renal arterial pressure (RAP) including renal blood flow, glomerular filtration rate, urine flow, sodium excretion, and fractional excretion of sodiumsurrogate

Intra-arterial administration of a nitric oxide donor restores renal blood flow and sodium excretion in dogs with inhibited endogenous nitric oxide synthesis.

Cite This Study

Majid et al. (1993) studied this question.

synapsesocial.com/papers/6a87367ce0e6abca40d3cbc1 https://doi.org/10.1161/01.hyp.22.4.535

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