July 1, 2001AJP Heart and Circulatory Physiology
Differential ANG II-induced growth activation pathways in mesenteric artery smooth muscle cells from SHR
Key result
Angiotensin II stimulates VSMC proliferation via AT1 and AT2 receptors in SHR, whereas it induces hypertrophy via AT1 receptors in WKY rats, mediated by ERK1/2-dependent pathways.
Population
Vascular smooth muscle cells from mesenteric arteries of spontaneously hypertensive and Wistar-Kyoto rats
Comparison
Angiotensin II vs Responses between SHR and WKY strains, and…
Design
Preclinical
Authors
Discussion
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Implication
Suggests model-specific vascular responses; leaves open clinical relevance of AT receptor targeting in human hypertension.
Structured PICO
P
Population
In vitro study of vascular smooth muscle cells from mesenteric arteries of spontaneously hypertensive and Wistar-Kyoto rats.
I
Intervention
Angiotensin II (with and without inhibitors: losartan, PD-123319, PD-98059, LY-294002, bisindolylmaleimide)
C
Comparator
Responses between SHR and WKY strains, and baseline/untreated cells
O
Outcome
Protein synthesis ([(3)H]leucine incorporation) and DNA synthesis ([(3)H]thymidine incorporation)surrogate
Angiotensin II induces differential growth activation pathways in vascular smooth muscle cells of hypertensive versus normotensive rats, potentially contributing to vascular remodeling.
Cite This Study
Mabrouk et al. (2001) studied Hypertension. Angiotensin II vs. Various receptor antagonists and kinase inhibitors was evaluated on Protein synthesis, DNA synthesis, and ERK1/2 activation. Angiotensin II stimulates VSMC proliferation via AT1 and AT2 receptors in SHR, whereas it induces hypertrophy via AT1 receptors in WKY rats, mediated by ERK1/2-dependent pathways.