It is widely accepted that excess salt intake is a risk factor for development of hypertension [1,2]. Current research also supports the idea that adverse conditions during pregnancy can affect progeny postnatal health, both immediately after birth and for the remainder of their lives [3,4]. The purpose of this mini review is to discuss the effects of a gestational high-salt diet on renal development and programming of the renin angiotensin system in the fetus and how these changes increase the offspring’s incidence of hypertension and renal disease later in life. After reviewing a large body of evidence collected from and related to maternal high-salt diet experiments, it is proposed that high salt (HS) diet during pregnancy causes an increased prevalence of hypertension in offspring due to {A} an overall increase in blood pressure resulting from absence of appropriate modulation of plasma renin activity in response to changes in salt concentration, {B} an increased pressor response to angiotensin II, and {C} a decrease in the number of glomeruli per kidney. (Figure 1) provides a summary of the pathophysiological changes in the fetus caused by maternal high HS diet, and how these changes lead to an increase in the rate of disease risk in offspring.