Since blood pressure is lower in pendrin null than in wild type mice, reduced vascular tone is expected. GSK2269557 However, pendrin null mice have elevated plasma renin concentration, which should increase plasma angiotensin II concentration, thereby stimulating vascular contractility. To resolve these issues, the effect of pendrin ablation on vascular reactivity was examined in aortic rings. The purpose of this study was threefold: 1) to determine if pendrin is expressed in mouse aorta, 2) to determine if the lower blood pressure THZ1 observed in pendrin null mice occurs in tandem with reduced vascular contractile function and 3) to ascertain the mechanism by which this occurs. Following 7 days of the NaCl-replete diet employed in this study, we observed previously that mean arterial pressure measured by telemetry is lower in pendrin null than in wild type mice. Further experiments asked if the fall in blood pressure observed with pendrin gene ablation occurs in tandem with reduced vascular reactivity. Further experiments examined force development normalized to cross sectional area in thoracic aortas from pendrin null and wild type mice. In response to KCl, force generation/cross sectional area trended higher in the pendrin null relative to the wild type aorta, although differences did not reach statistical significance. However, in response to phenylephrine, force/cross-sectional area was increased in the pendrin null relative to the wild type aorta. Because pendrin gene ablation increased force when normalized to cross sectional area, we compared cross sectional area in the thoracic aorta from mice in each group. As shown, cross sectional area was lower in aortas from pendrin null relative to wild type mice. Similarly, aorta intima and media thickness quantified by planar morphometry was lower in pendrin null than in wild type mice, which is consistent with the 11% lower body weight observed in the pendrin null relative to wild type mice. We conclude that the enhanced force/per cross sectional area observed in the pendrin null aorta was primarily due to reduced cross-sectional area rather than increased force/vessel.