There is direct and indirect evidence that the kidneys are involved in the onset of hypertension in spontaneously hypertensive animals. In the Dahl strain, rather convincing evidence exists for a primary, inherent renal defect that is worsened by high dietary salt. In the Okamoto and New Zealand strains, an intrinsic defect may be provoked by increased sympathetic nerve activity. Similarities between all of these strains and Goldblatt hypertension suggest a fluid volume abnormality, but the gradual onset of elevated pressure and continuing growth during development of hypertension may obscure critical volume changes. Theoretically, arterial pressure, somewhat independent of intermediate steps, will reach the level which is dictated by renal function as being necessary for the maintenance of salt and water homeostasis. While widespread use of different spontaneously hypertensive strains may currently be complicating our understanding of the intermediate steps, studies of dissimilar strains should, in time, enhance our understanding of the many different facets of long-term blood pressure control.