Abstract
Recently, attention has been given to a hyperresponsiveness to vasopressor agents in various forms of hypertension. Hypertrophy and/or “water-logging” of blood vessels associated with prolonged hypertension has been found to narrow vessel lu-mina and lead to such hyperresponsiveness (1). In addition, subnormal mono-amine oxidase activity accompanied by increased tissue norepinephrine concentration has been reported in genetically hypertensive turkeys, which also exhibited a greater vasopressor response to exoge-nously administered norepinephrine (2).Lately there has been a renewed interest in a “sensitizing factor” to catechol-amines in hypertension, but because of the diverse nature of some studies and the frequent utilization of inadequate controls, reports have been conflicting. Several investigators have found evidence for a vasopressor agent potentiating factor among hypertensive subjects (3-6), and a transmittable humoral factor has been suggested by a study that utilized the par-abiotic union of a ...
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