In addition, changes in cardiac sympathetic activity do not appear to contribute to hypertension in this model since neither chronic administration of the beta‐1 adrenoceptor antagonist, atenolol, or denervation of cardiac sympathetic nerves by stellate ganglionectomy affect the arterial pressure or heart response to AngII in high‐salt rats (Hirsch and Osborn 2011). The gene discussed is AGT; the disease is hypertensive disorder.