ABSTRACT
It is sometimes asserted that primary (essential) hypertension is fundamentally a genetically-determined disorder, and that environmental and behavioral stress factors play little or no role in the pathogenetic process (Genest, 1977). The fact that a positive familial history of hypertension is a risk factor for hypertension is consistent with this formulation, as is the fact that strains of rats have been bred which become hypertensive “spontaneously” (Okamoto & Aoki, 1963). The genetic hypothesis also appears to be supported by observations of the effectiveness of internal autoregulatory systems which operate to restore homeostatic levels following acute elevations of blood pressure induced by environmental events. As long as they function properly, autoregulatory systems should be able to prevent chronic elevations in blood pressure. Certainly one of the most important of these systems is the kidney, which continuously adjusts circulating fluid levels via excretion of water and sodium to maintain blood pressure within normotensive limits (Guyton, 1980). According to this traditional view, primary hypertension evolves in response to genetically-programmed malfunction of one or more of the autoregulatory systems.
