What question did this study set out to answer?

The research aims to investigate the roles of angiotensin II type 1a receptors in regulating blood pressure and renin gene expression.

August 1, 1995Journal of Biological ChemistryOpen Access

Angiotensin II Type 1a Receptor-deficient Mice with Hypotension and Hyperreninemia

Q: What is the clinical evidence from this study?

Population: Hypotension and hyperreninemia. Intervention: AT1a receptor deficiency vs. Wild-type littermates. Primary outcome: Systolic blood pressure (10 and 22 mm Hg lower).

View Full Paper

Ask AI

Bookmark

Key result

AT1a receptor-deficient mice exhibited chronic hypotension, with systolic blood pressure 10 and 22 mm Hg lower in heterozygous and homozygous mutants, respectively, than in wild-type littermates.

Population

Mice with a targeted replacement of the AT1a receptor loci by the lacZ gene and wild-type littermates

Comparison

Targeted replacement of the AT1a receptor loci… vs Wild-type littermates

Design

Preclinical

Authors

TSTakeshi SugayaSt. Marianna University School of Medicine SNShin‐ichiro NishimatsuKawasaki Medical School KTKeiji TanimotoUniversity of Tsukuba

Discussion

Member takes

Implication

AT1a receptor is essential for BP homeostasis in mice; leaves open translation to human hypertension therapies.

Key Points

The research aims to investigate the roles of angiotensin II type 1a receptors in regulating blood pressure and renin gene expression.
Generated mutant mice with a targeted replacement of the AT1a receptor loci.
Assessed blood pressure and renin levels in both heterozygous and homozygous mutant mice compared to wild-type.
Measured lacZ staining in renal structures to validate receptor activity.
Heterozygous mutant mice showed a 10 mm Hg reduction in systolic blood pressure compared to wild-type.
Homozygous mutant mice exhibited a 22 mm Hg decrease in systolic blood pressure and marked increases in renin mRNA levels and plasma renin activity.
Findings suggest an AT1a-mediated pathway is significantly involved in blood pressure regulation and renin gene expression.

Structured PICO

Population

Mice with a targeted replacement of the AT1a receptor loci by the lacZ gene (heterozygous and homozygous mutant mice) and wild-type littermates

Exposure

Targeted replacement of the AT1a receptor loci by the lacZ gene (AT1a receptor deficiency)

Comparator

Wild-type littermates

Outcome

Systolic blood pressure, renin mRNA levels in the kidney, and plasma renin activitysurrogate

Main Result

Effect estimate: 10 and 22 mm Hg lower

Targeted disruption of the AT1a receptor in mice results in chronic hypotension and hyperreninemia, confirming its critical role in blood pressure regulation.

Cite This Study

Sugaya et al. (1995) studied Hypotension and hyperreninemia. AT1a receptor deficiency vs. Wild-type littermates was evaluated on Systolic blood pressure (10 and 22 mm Hg lower). AT1a receptor-deficient mice exhibited chronic hypotension, with systolic blood pressure 10 and 22 mm Hg lower in heterozygous and homozygous mutants, respectively, than in wild-type littermates.

synapsesocial.com/papers/6a1f2142cf1cd4bd52914daf https://doi.org/10.1074/jbc.270.32.18719

View Full Paper

Ask AI

Bookmark

Angiotensin II Type 1a Receptor-deficient Mice with Hypotension and Hyperreninemia

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Angiotensin II Type 1a Receptor-deficient Mice with Hypotension and Hyperreninemia

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider