We examined the arterial phenotype of mice lacking 1 integrin (1-/-) at baseline and after 4 weeks of angiotensin II (Ang II) or norepinephrine (NE) administration. Arterial mechanical properties were determined in the carotid artery (CA). Integrin expression, MAPK kinases and focal adhesion kinase were assessed in the aorta. No change in arterial pressure was observed in 1-/- mice. Elastic modulus-wall stress curves were similar between 1-/- and 1+/+ animals, indicating no change in arterial stiffness. The rupture pressure was lower in 1-/- mice, demonstrating decreased mechanical strength. Lack of 1 was accompanied by an increase in integrins1, v and 5, without any change in 2 integrin. Ang II increased medial cross-sectional area of the CA in 1+/+ but not in 1-/- mice, whereas equivalent pressor doses of NE did not produce significant increases in either group. In 1+/+ mice, Ang II induced both 1 expression and smooth muscle cell (SMC) hypertrophy in the CA associated with increased aortic expression of -smooth muscle actin (-SMA), smooth muscle myosin heavy chain (SM-MHC), phosphorylation of ERK1/2, p38 MAPK and FAK. Ang II did not induce SMC hypertrophy or phosphorylation of p38MAPK and FAK in 1-/- mice. A functional anti-1 antibody inhibited in vitro the Ang II-induced phosphorylation of FAK and p38 MAPK. In conclusion, 1-/- mice exhibit a reduced mechanical strength at baseline and a lack of Ang II-induced SMC hypertrophy. These results emphasize the importance of 11 integrin in p38MAPK and FAK phosphorylation during vascular hypertrophy in response to Ang II.