November 6, 2015Arteriosclerosis Thrombosis and Vascular Biology

Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice

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Population

Mice with genetically upregulated eNOS activity and wild-type mice

Comparison

Genetic upregulation of eNOS activity and… vs Wild-type mice

Design

Preclinical

Authors

SGShigeo GodoTohoku University ASAyuko SawadaTohoku University HSHiroki SaitoTohoku University

Discussion

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Implication

Excessive endothelial NO may worsen pressure-overload outcomes in mice; leaves open Cav-1/eNOS targeting in human cardiomyopathy.

Structured PICO

Population

Mice with genetically upregulated eNOS activity (Cav-1-knockout [Cav-1-KO] and endothelium-specific eNOS transgenic [eNOS-Tg] mice) and wild-type mice

Intervention

Genetic upregulation of eNOS activity (Cav-1-KO and eNOS-Tg) and chronic pressure overload by transverse aortic constriction

Comparator

Wild-type mice

Outcome

Cardiovascular homeostasis (including NO-mediated and EDH-mediated relaxations, cardiac hypertrophy, hypotension, and survival after transverse aortic constriction)surrogate

Excessive endothelium-derived NO with reduced EDH impairs cardiovascular homeostasis and worsens outcomes following chronic pressure overload in mice.

Cite This Study

Godo et al. (2015) studied this question.

synapsesocial.com/papers/6a7c183a0bfa86fad9c6635d https://doi.org/10.1161/atvbaha.115.306499

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Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Disruption of Physiological Balance Between Nitric Oxide and Endothelium-Dependent Hyperpolarization Impairs Cardiovascular Homeostasis in Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider