Integrin α1 knockout mice (α1−/−) were used to investigate the role of the integrin α1β1 in the cardiac and vascular functions of angiotensin II (AngII)-induced hypertension. Carotid artery (CA) elasticity was measured by incremental elastic modulus (Einc)-wall stress curves using an ultrasonic echo-tracking device and the measurement of medial cross-sectional area (MCSA) to evaluate in vivo CA mechanical properties. Cardiac function was studied by echocardiography in anaesthetized animals.

Infusion of Ang II (200ng/kg/min) in α1−/− mice and their control (α1+/+) for 4 weeks led to similar hypertensive effect (SAP +31 vs +37 mmHg). In α1−/− Ang II failed to increase MCSA of CA whereas it did in α1+/+ mice. The Einc-stress curve of Ang II-treated α1−/− was shifted to the right compared to Ang II-treated α1+/+, indicating a decreased arterial stiffness. The α1+/+ had an increased cardiac hypertrophy, evaluated by an increase of the end diastolic thickness of the septum (IVSd: 1.2±1 vs 0.9±0.08 mm) without modification of the posterior wall (LVPWd: 0.10±0.6 vs 0.97±0.07 mm) and without dilation of the ventricular cavity. This septal hypertrophy was not found in the α1−/− mice in response to Ang II. Cardiac fibrosis measured by collagen quantification (total, and type I and III), was lower in the α1−/− mice, compared with the α1+/+.

In conclusion, our results show an impaired of cardiovascular response to Ang II-induced hypertension in the integrin α1 knockout mouse. These results suggest the involvement of this integrin in the cardiovascular effects of Ang II.