In the current study, salt-induced hypertension developed in two phases, early and late, which is typical for Dahl SS rats (Moreno et al., 2011; Evans et al., 2015). We observed an elevation in MAP and a progressive increase in day/night blood pressure dipping in all animals fed a high-salt diet, consistent with earlier findings (Mori et al., 2008; Cowley et al., 2016). In hypertensive and normotensive humans, nocturnal dipping is usually defined as a >10% decline in BP (Henskens et al., 2008) and has an important diagnostic significance: it has been shown that impaired BP dipping is associated with increased risk of cardiovascular events and target organ damage (Ohkubo et al., 2002; De La Sierra et al., 2009). In subjects from African descent, sodium excretory renal function during daytime was found to be a significant determinant of nocturnal BP and dipping (Bankir et al., 2008), whereas salt-resistant normotensive individuals' BP was not blunted on standard and high-sodium diets (Brian et al., 2017). Also, metabolic syndrome is recognized as a predictor of non-dipping hypertension (Tartan et al., 2006), and we expected that targeting AMPK activity might have an effect on circadian dipping in Dahl SS rats. However, in the current study blood pressure elevation was not accompanied by impaired dipping in either vehicle- or drug-treated animals. High-salt diet also substantially increased the activity of AMPK in the kidney cortex as revealed by Western blotting. We further tested whether treatment with the AMPK activators metformin and AICAR (given via intravenous infusion) affects the development of hypertension.