What question did this study set out to answer?

To determine whether the selective p38 MAPK inhibitor SB239063AN attenuates Angiotensin II-induced hypertension, end-organ damage, and superoxide anion production in vivo.

June 1, 2007Journal of Cardiovascular Pharmacology

Effects of p38 MAPK Inhibitor on Angiotensin II-Dependent Hypertension, Organ Damage, and Superoxide Anion Production

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Why the study?

Does p38 MAPK inhibition with SB239063AN attenuate Angiotensin II-dependent hypertension, organ damage, and reactive oxygen species production in animal models?

Key Points

To determine whether the selective p38 MAPK inhibitor SB239063AN attenuates Angiotensin II-induced hypertension, end-organ damage, and superoxide anion production in vivo.
Infused Sprague-Dawley rats and MAPKAP kinase-2 knockout mice with Angiotensin II to induce vascular and cardiac pathology.
Administered the orally active, selective p38 MAPK inhibitor SB239063AN at 800 ppm in the diet.
Angiotensin II infusion increased phosphorylated p38 MAPK, raised aortic superoxide anion production 4-fold, and elevated gp91 mRNA expression 5-fold while inducing endothelial dysfunction, hypertension, and cardiac hypertrophy.
SB239063AN treatment significantly reduced superoxide anion generation by 57% (P < 0.01), suppressed gp91 expression, restored endothelial function, and blunted hypertension and cardiac hypertrophy.
Angiotensin II-dependent hypertension was also significantly attenuated in MAPKAP kinase-2 knockout mice.

Structured PICO

Does p38 MAPK inhibition with SB239063AN attenuate Angiotensin II-dependent hypertension, organ damage, and reactive oxygen species production in animal models?

Population

Sprague-Dawley rats and MAPKAP kinase-2 knockout mice infused with Angiotensin II

Intervention

SB239063AN (800 ppm in the diet), a highly selective, orally active p38 MAPK inhibitor

Comparator

Angiotensin II infusion without p38 MAPK inhibitor

Outcome

Superoxide anion generation, gp91 mRNA expression, endothelial dysfunction, hypertension, and cardiac hypertrophysurrogate

Inhibition of p38 MAPK attenuates Angiotensin II-induced hypertension, cardiac hypertrophy, and oxidative stress in animal models, suggesting a potential therapeutic target for cardiovascular disease.

Discussion

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Implication

Hypothesis-generating for p38 MAPK inhibition in experimental hypertension; prospective human studies needed before any clinical consideration.

Cite This Study

Bao et al. (2007) studied this question.

synapsesocial.com/papers/6a79737074c579e25f88fe7c https://doi.org/10.1097/fjc.0b013e318046f34a

Topics

Hypertension management Echocardiography

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Implication

Hypothesis-generating for p38 MAPK inhibition in experimental hypertension; prospective human studies needed before any clinical consideration.

Effects of p38 MAPK Inhibitor on Angiotensin II-Dependent Hypertension, Organ Damage, and Superoxide Anion Production

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Topics

Effects of p38 MAPK Inhibitor on Angiotensin II-Dependent Hypertension, Organ Damage, and Superoxide Anion Production

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

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