Essential vascular hypertension seems to represent a pattern of inappropriate reaction to the stresses of living.1 The early stage of repeated transitory hypertensive responses is usually considered to reflect abnormal sympathetic nervous activity. As the disease progresses, this stage is succeeded by sustained elevation of systolic and diastolic pressures, associated with varying degrees of vascular damage, renal, myocardial and cerebral.2
The concept of adrenocortical involvement in sustained hypertension received impetus from Selye's detailed studies of reactions to stress.3 Before that time it was recognized that destruction or removal of the adrenal glands resulted in marked depression of blood pressure, while hyperplasia or tumor was associated with elevation of pressure. What appeared to have escaped general emphasis is the uniqueness of the adrenal gland as an organ in which hypofunction is intimately related to hypotension and hyperfunction to hypertension.
This fundamental relation to long term changes in pressure