We examined whether sugar-induced systolic blood pressure (SBP) elevations in rats may develop, in part, through a mechanism common to salt-induced hypertension, i.e., renal retention of water and salt.Spontaneously hypertensive rats (SHR) ate four diets: two high (>50% of calories) and two low (<12% of calories) in sugar (sucrose). SBP, various urinary parameters, and the renal angiotensin and prostaglandin systems were assessed.SHR consuming diets high in sugar showed significantly decreased urinary volume and excretion of electrolytes, which coincided with increasing SBP. When low sugar diets replaced high sugar diets, SBP and urinary parameters rapidly returned to baseline. SHR received captopril while consuming high sugar diets, and both SBP and urinary parameters assumed baseline values, comparable to ones seen in SHR consuming low sugar diets. A direct angiotensin II receptor antagonist (DuPont 753) did not influence SBP. However, we found decreased PGE2 excretion in SHR consuming excess sugar.Salt and water retention occur early during sugar-induced hypertension due to reduced renal excretion, consistent with some part in the pathogenesis. The effects of high sugar diets on SBP were not due to angiotensin II inhibition, however, decreased availability of vasodilatory prostaglandins may play a role in the renal events and sugar-induced hypertension in SHR.