March 1, 2001Journal of Hypertension
Differential activation of extracellular signal-regulated protein kinase 1/2 and p38 mitogen activated-protein kinase by AT1 receptors in vascular smooth muscle cells from Wistar–Kyoto rats and spontaneously hypertensive rats
Population
Vascular smooth muscle cells from mesenteric arteries of Wistar-Kyoto rats and spontaneously hypertensive rats
Comparison
Angiotensin II vs WKY rats vs SHR, and presence vs absence of…
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating for AT1-driven MAPK hyperactivation in hypertensive vessels; leaves open translation to human disease and therapy.
Structured PICO
P
Population
Vascular smooth muscle cells (VSMC) from mesenteric arteries of Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR)
I
Intervention
Angiotensin II (with or without inhibitors: irbesartan, PD123319, PP2, PD98059, SB202190)
C
Comparator
WKY rats vs SHR, and presence vs absence of inhibitors
O
Outcome
Phosphorylation of ERK1/2, JNK, and p38MAPK; c-fos mRNA expressionsurrogate
Angiotensin II induces increased activation of ERK1/2 and p38MAPK via AT1 receptors in vascular smooth muscle cells from spontaneously hypertensive rats, suggesting a role in altered growth signaling.
Cite This Study
Touyz et al. (2001) studied this question.