The myogenic response of afferent arterioles is a key autoregulatory mechanism that protects the glomeruli from barotrauma. Afferent arteriolar smooth muscle cells contract to increased intraluminal pressure through mechanosensitive cation channels and interactions between integrin and extracellular matrix that trigger calcium-dependent actomyosin contraction. The study by Feng et al. provides evidence supporting the concept that increased matrix metalloproteinase 9 in kidney microvessels of Dahl salt-sensitive rats interferes with integrin-matrix binding and promotes phenotypic transformation of afferent arterioles, causing loss of myogenic constriction and hypertensive nephropathy.