ALL chronic hypertensive states in human subjects manifest some renal or adrenal alterations, or both. Persistently elevated systemic blood pressures damage the delicate intrarenal and periadrenal arterioles to produce the familiar arteriolosclerotic changes and eventually varying degrees of parenchymal degeneration and atrophy with stromal fibrosis result.
More cogent diagnostic and therapeutic problems than those provided by renal and adrenal lesions secondary to chronic hypertension are (1) the relatively uncommon primary renal or adrenal abnormalities responsible for increased blood pressures and (2) the renal or adrenal alterations that may secondarily exaggerate or maintain any hypertensive state.
Primary Renal Hypertension
Goldblatt's renal arterial clamping experiments are mirrored by the natural human condition in which either parts or all of one or both kidneys are served by stenotic renal arteries.1 Quantitative determinations have not been made of the precise range of cross-sectional narrowing required to set off the Goldblatt mechanism. Usually the