Higher levels of inflammatory mediators, in particular TNF‐α, were found in the kidney in cisplatin renal injury (Deng et al., 2001; Ramesh & Reeves, 2002, 2004; Zhang et al., 2007) as well as other renal injury and hypertension models including the deoxycorticosterone acetate (DOCA) hypertension model (Banek et al., 2016; Elmarakby et al., 2008), angiotensin II‐induced hypertension (Guzik et al., 2007) and salt‐sensitive hypertension (Huang et al., 2016) indicating a possible role of these mediators in initiating a sympatho‐excitatory response leading to impaired blood pressure homeostasis. This evidence concerns the gene TNF and hypertensive disorder.