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.