Renal vasculature in essential hypertension: a review of some contrarian evidence.

This chapter reviews a body of evidence concerning the anatomic pathology, pathogenesis, epidemiology and possible etiologic agents of benign essential hypertension in human populations. A core finding serves as the starting point for further reasoning: intimal fibroplasia of renal interlobular arteries (arteriosclerosis) increases with age at varying rates in all populations around the world, and the rise of mean arterial pressure (MAP) with age is closely tied to this process. The weight of evidence favors the view that fibroplasia progresses for wholly unknown reasons, is not accelerated by elevations in MAP, and that it raises MAP in proportion to its severity by creating nephron heterogeneity that initiates Goldblatt mechanisms. This form of hypertension has been designated type 2 to distinguish it from a less common form, called type 1, where the fibroplasia is of mild or minimal degree. This chapter reviews evidence that indicates type 1 does not evolve into type 2 because hypertension is not accelerating the process.Experimental models of hypertension include the Goldblatt model, which resembles some aspects of type 2, and spontaneous genetic models, which mimic some aspects of type 1 hypertension. There is currently no persuasive evidence that type 2 hypertension, as it naturally develops in the human during aging of 50 years or more, can be reproduced in laboratory animals. Clues to the etiology of the arterial fibroplasia that appears to underlie most instances of essential hypertension would best be sought in the study of variations among human populations around the world, and especially of their migrants.