Increased calcium influx, augmented sarcoplasmic reticular calcium release and decreased sarcoplasmic reticular calcium reuptake, activation of the PLC-DAG-IP3 pathway, increased calcium signalling, vascular hyperreactivity, and exaggerated contractile responses to vasoactive agonists have been demonstrated in genetic [spontaneously hypertensive rats (SHRs), stroke-prone SHR], experimental (deoxycorticosterone acetate (DOCA)-salt, Ang II-infused, L-NAME-induced), and human hypertension.47–54. This evidence concerns the gene AGT and Hypertension.