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