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Am J Physiol Heart Circ Physiol 281: H30-H39, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 1, H30-H39, July 2001

Differential ANG II-induced growth activation pathways in mesenteric artery smooth muscle cells from SHR

Mohammed El Mabrouk, Rhian M. Touyz, and Ernesto L. Schiffrin

Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada H2W 1R7

Angiotensin II-induced growth signaling mechanisms were investigated in vascular smooth muscle cells (VSMCs) from mesenteric arteries of sponteneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). In WKY, angiotensin II significantly increased protein synthesis ([3H]leucine incorporation) but not DNA synthesis ([3H]thymidine incorporation). In SHR, angiotensin II increased protein and DNA synthesis. VSMCs from both strains expressed angiotensin type 1 (AT1) and type 2 (AT2) receptors. Losartan (an AT1 receptor antagonist) but not PD-123319 (an AT2 receptor antagonist) attenuated angiotensin II-stimulated protein synthesis in WKY VSMCs. In SHR, losartan and PD-123319 partially inhibited angiotensin II-induced VSMC proliferation. The mitogen-activated protein kinase or extracellular signal-regulated protein kinase (ERK) kinase inhibitor PD-98059 blocked VSMC growth responses to angiotensin II in both strains. Angiotensin II increased ERK1/2 activation more in SHR than WKY, an effect inhibited by losartan but not PD-123319. LY-294002 [a phosphatidylinositol-3 (PI3) kinase inhibitor] blocked angiotensin II-stimulated ERK1/2 activation in SHR but not in WKY, whereas bisindolylmaleimide [a protein kinase C (PKC) inhibitor] was ineffective. In conclusion, angiotensin II stimulates VSMC proliferation via AT1 and AT2 receptors in SHR. In WKY, angiotensin II induces VSMC hypertrophy via AT1 receptors. ERK1/2-dependent pathways regulated by intracellular Ca2+ but not PKC mediate these effects. In SHR VSMCs, PI3 kinase plays a role in augmented angiotensin II-induced ERK1/2 phosphorylation. These angiotensin II-mediated signaling events could contribute to vascular remodeling in SHR.

hypertrophy; renin-angiotensin system; signal transduction; hypertension


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