Etiological Classification of Hypertension

Summary

In this paper, I shall present an overview of major studies on hypertension and propose a new etiological classification. Since the 1800s, investigators have questioned the concept, mechanism, and classification of hypertension in humans and animals. Bright reported hypertension as a renal disease. Gull and Sutton distinguished hypertension from renal disease. Albutt, Frank, and others assumed that subjects with essential hypertension differed qualitatively from subjects with normotension. Pickering rejected that essential hypertension was a specific disease entity and proposed that essential hypertension should be the name given to the syndrome of a group of subjects with high blood pressure caused by polygenic inheritance. Platt suggested that essential hypertension was the manifestation of a single gene inheritance. The values of the genetic parameters were calculated from the variance of crossbreedings of the spontaneously hypertensive rat (SHR), which demonstrated that the inheritance of hypertension in the SHR might be the incomplete dominant form transferred by three major genes and not completely polygenic. There are three qualitatively different kinds of hypertension animal models, including Aoki SHR of major gene hypertension, Dahl salt-sensitive rats of environment (accessory gene) hypertension, and Goldblatt renal hypertension animals of disease-induced (nongene) hypertension. On the basis of animal models and investigations of human hypertension, we have proposed an etiological classification in humans and animals as follows: Type 1, essential (major gene) hypertension; type 2, environment (accessory gene) hypertension; and type 3, disease (nongene) hypertension. This classification may be useful in the research on mechanisms, treatment, and prevention of hypertension.