The Rho-kinase inhibitor, fasudil, can reverse vasoconstriction induced by ET-1 [29] and serotonin [30] and attenuate angiotensin II- (AII-) induced cardiac hypertrophy [31] and endothelin- (ET-) induced cardiac myocyte hypertrophy [32], and the potent vasoconstrictors including AII [33], ET [29], and serotonin [34] can activate the Rho/Rho-kinase pathway. This evidence concerns the gene NLRP3 and cardiac hypertrophy.