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January 28, 2014Journal of Receptors and Signal Transduction

Angiotensin II and Angiotensin III caused a rapid, dose-dependent increase in p38 MAP kinase phosphorylation in cultured rat astrocytes, with Ang II being almost twice as potent as Ang III.

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Population

Cultured rat brainstem astrocytes

Design

Preclinical

Follow-up

minutes

Key result

Angiotensin II and Angiotensin III caused a rapid, dose-dependent increase in p38 MAP kinase phosphorylation in cultured rat astrocytes, with Ang II being almost twice as potent as Ang III.

Authors

AAAhmed Z. AlanaziPPParas PatelMCMichelle A. Clark

Discussion

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Overview

No immediate clinical implications; extends prior astrocyte MAP kinase data to p38 but leaves relevance open.

Structured PICO

P
Population
Cultured rat brainstem astrocytes
I
Intervention
Angiotensin II and Angiotensin III
O
Outcome
p38 MAP kinase protein phosphorylationsurrogate

Angiotensin II and III directly stimulate p38 MAP kinase phosphorylation in rat astrocytes via the AT1 receptor, providing insight into the molecular mechanisms of these peptides in the brain.

Cite This Study

Alanazi et al. (2014) studied this question. Angiotensin II and Angiotensin III was evaluated on p38 MAP kinase phosphorylation. Angiotensin II and Angiotensin III caused a rapid, dose-dependent increase in p38 MAP kinase phosphorylation in cultured rat astrocytes, with Ang II being almost twice as potent as Ang III.

synapsesocial.com/papers/6a6ba6f934b735385cb3c9cfhttps://doi.org/10.3109/10799893.2013.876041
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