October 1, 2001AJP Renal Physiology

Genetic disruption of atrial natriuretic peptide receptor-A alters renin and angiotensin II levels

Q: What is the clinical evidence from this study?

Study design: Other. Population: Npr1 gene disruption. Intervention: Npr1 gene disruption (0-copy mutant) vs. 2-copy wild-type (+/+) animals. Primary outcome: Baseline systolic arterial pressure (SAP).

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Key result

Npr1 gene disruption in 0-copy mutant mice resulted in significantly higher baseline systolic arterial pressure (143 +/- 2 mmHg) compared to 2-copy wild-type animals (104 +/- 2 mmHg).

Population

Npr1 gene-disrupted mutant mouse model

Comparison

Npr1 gene disruption vs 2-copy wild-type (+/+) mice

Design

Preclinical

Authors

SSShang‐Jin ShiNational Aeronautics and Space Administration HNHuong Thanh NguyenWayne State University GSGuru Dutt SharmaTulane University

Discussion

Member takes

Implication

Npr1 gene dosage modulates BP in mice; leaves open translational relevance to human hypertension and RAAS.

Structured PICO

Population

Male mice (newborn, young, and adult) with 0-copy, 1-copy, and 2-copy Npr1 gene disruption to study cardiovascular and renal phenotypes.

Exposure

Npr1 gene disruption (0-copy mutant -/- and 1-copy heterozygote +/-)

Comparator

2-copy wild-type (+/+) mice

Outcome

Systolic arterial pressure and components of the renin-angiotensin-aldosterone system (RAAS) in plasma, kidney, and adrenal glandsurrogate

Main Result

Absolute Event Rate: 143% vs 104%

Genetic disruption of the NPRA receptor in mice leads to elevated blood pressure and age-dependent alterations in the renin-angiotensin-aldosterone system, suggesting NPRA activation directly inhibits renin.

Cite This Study

Shi et al. (2001) studied Npr1 gene disruption. Npr1 gene disruption (0-copy mutant) vs. 2-copy wild-type (+/+) animals was evaluated on Baseline systolic arterial pressure (SAP). Npr1 gene disruption in 0-copy mutant mice resulted in significantly higher baseline systolic arterial pressure (143 +/- 2 mmHg) compared to 2-copy wild-type animals (104 +/- 2 mmHg).

synapsesocial.com/papers/6a657e69d0b9f96261fe585f https://doi.org/10.1152/ajprenal.2001.281.4.f665

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October 1, 2001AJP Renal Physiology

Genetic disruption of atrial natriuretic peptide receptor-A alters renin and angiotensin II levels

View Full Paper

Ask AI

Bookmark

Key result

Npr1 gene disruption in 0-copy mutant mice resulted in significantly higher baseline systolic arterial pressure (143 +/- 2 mmHg) compared to 2-copy wild-type animals (104 +/- 2 mmHg).

Population

Npr1 gene-disrupted mutant mouse model

Comparison

Npr1 gene disruption vs 2-copy wild-type (+/+) mice

Design

Preclinical

Authors

SSShang‐Jin ShiNational Aeronautics and Space Administration HNHuong Thanh NguyenWayne State University GSGuru Dutt SharmaTulane University

Discussion

Member takes

Implication

Npr1 gene dosage modulates BP in mice; leaves open translational relevance to human hypertension and RAAS.

Structured PICO

Population

Male mice (newborn, young, and adult) with 0-copy, 1-copy, and 2-copy Npr1 gene disruption to study cardiovascular and renal phenotypes.

Exposure

Npr1 gene disruption (0-copy mutant -/- and 1-copy heterozygote +/-)

Comparator

2-copy wild-type (+/+) mice

Outcome

Systolic arterial pressure and components of the renin-angiotensin-aldosterone system (RAAS) in plasma, kidney, and adrenal glandsurrogate

Main Result

Absolute Event Rate: 143% vs 104%

Cite This Study

synapsesocial.com/papers/6a657e69d0b9f96261fe585f https://doi.org/10.1152/ajprenal.2001.281.4.f665

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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