[Role of extracellular matrix in angiotensin II signalling in aortic smooth muscle cells: relationship with arterial hypertension].

Angiotensin II (Ang II) is involved in hypertension-related arterial wall hypertrophy [1]. Regulation of AT II transduction pathway in vascular smooth muscle cells (VSMC) may involve cytoskeleton and extracellular matrix (ECM) [2]. We assessed the role of components of ECM on Ca i 2+ increase induced by Ang II in Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR) aortic VSMC. The effect of Ang II (1 pmol) on Ca 2+ mobilization was studied in cultured VSMC isolated from the aorta of 6-wk old WKY (MAP (m±SE)=98±4 mmHg) and SHR (136±5 mmHg; p<0.05), using fluorescent imaging microscopy (Fura-2 AM). Ca i 2+ release from internal stores and Ca 2+ influx were assessed in the absence and upon reintroduction of external Ca 2+ respectively. Cells were cultured on uncoated glass coverslips (control) or coated with either collagen I (10 μg/mL), collagen IV (7 μg/mL), vitronectin (0.1 μg/mL), fibronectin (3 μg/mL) and extracellular matrix extract (matrigel, 1/10) and studied at confluence. Paxillin was located in cells by indirect immunofluorescence micrography. Results are expressed in % of Control. Statistical significance (p<0.05) was assessed with Student's t-test for unpaired data. The effects on Ang II-induced Ca 2+ mobilization of growing cells on ECM are in Table. Paxillin in Control cells appeared as dots at the cell boundaries. Density increased in cells grown on collagen I with a diffuse distribution in the WKY cells. On matrigel, paxillin was located in a belt-like fashion at the periphery of the cell. These effects were not linked to differences in cell cycle (flux cytometry).