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 proper! y, 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.