A new study has shown that targeted disruption of the Adamts16 gene in a rat model of hypertension resulted in a reduction in systolic blood pressure and vascular media thickness, a lowering of aortic pulse wave velocity, a lengthening of mechanosensory cilia on vascular endothelial cells, the splitting and thickening of glomerular capillaries, and an increase in survival time. The researchers suggest that Adamts16 might act on the vasculature to regulate blood pressure.