Certain things have not changed since my colleague and I last reviewed the role of dietary salt in hypertension [Haddy, F.J., Pamnani, M.B., 1995. Role of dietary salt in hypertension. Journal of the American College of Nutrition 14, 428-438]. Over half of hypertensives are still salt sensitive, i.e., they respond to a high NaCl intake with a rise in blood pressure. This can be ameliorated by restricting NaCl intake, supplementing potassium intake, and consuming diuretics. Some things have changed. We now have more insight into mechanism; we suspected that volume expansion and endogenous Na(+),K(+)-ATPase inhibitors were the connection between excessive salt intake and the hypertension, but we were not certain as to the nature of the inhibitors. Now it appears that the inhibitors are steroids released from the adrenal gland and are members of the cardenolide family, e.g., ouabain, and the bufadienolide family, e.g., marinobufagenin. This presents new possibilities in therapy, including antibodies to these agents and competitive inhibitors to their binding to Na(+),K(+)-ATPase.