In contrast, the enhanced BP reduction elicited by acute fasudil administration to intact rats with either type of experimental hypertension might be ascribed either to the augmentation of RhoA/Rho kinase signaling in hypertensive animals by their sympathetic hyperactivity or to insufficient compensation of fasudil-induced BP fall due to the impaired baroreflex efficiency in hypertensive rats. This evidence concerns the gene RHOA and hypertensive disorder.