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(Hypertension. 2001;37:1465.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Effect of Extracellular Matrix Elements on Angiotensin II–Induced Calcium Release in Vascular Smooth Muscle Cells From Normotensive and Hypertensive Rats

Hélène Bouillier; Emmanuel Samain; Catherine Rücker-Martin; Jean-François Renaud; Michel Safar; Georges Dagher

From INSERM U337 (H.B., E.S., M.S.) and INSERM U465 (G.D.), Faculty Broussais-Hotel Dieu; and CNRS, Marie Lannelongue Hospital (H.B., E.S., C.R.-M., J.-F.R.), Paris, France.

Correspondence to Michel Safar, Hôpital Broussais, Service de Médecine Interne 1.0, 96 rue Didot, 75014 Paris, France.

Abstract—The interaction of the vascular smooth muscle cells (VSMCs) with the components of the matrix determines several functions of the cell, such as growth and differentiation. In contrast, an alteration in angiotensin (Ang) II–induced Ca²⁺ mechanisms in VSMCs was reported in genetic hypertension. In this study, we wished to assess the effect of different components of the extracellular matrix on the increase of [Ca²⁺]_i induced by Ang II in VSMCs from spontaneously hypertensive rats (SHR) compared with those from normotensive Wistar-Kyoto rats (WKY). Results demonstrate for the first time that elements of the extracellular matrix modulate the Ang II–induced Ca²⁺ transport mechanisms. This modulation is different in cells from WKY compared with those from SHR. Thus, growing cells from SHR on collagen I, collagen IV, fibronectin, vitronectin, or Matrigel induced a significant decrease in Ang II–induced Ca²⁺ release from internal stores, whereas in cells from WKY, no effect could be observed except for those grown on collagen I, which increased Ca²⁺ release. Fibronectin and vitronectin, however, induced a decrease in Ang II–induced Ca²⁺ influx in WKY, whereas no effect could be observed in SHR. Conversely, collagen I and collagen IV induced an increase in this influx in SHR but not in WKY, whereas Matrigel increased the influx in both strains. These results suggest a modulation of the Ang II–associated signaling events by the matrix elements via the focal adhesion points. The understanding of these synergies should provide insight into issues such as development of hypertrophy of large vessels in hypertension.

Key Words: extracellular matrix • collagen • fibronectin • vitronectin • angiotensin II • muscle, smooth, vascular • calcium

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