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 strain of rats that was genetically susceptible to the development of hypertension (7). In addition, a blood-borne factor in hypertensive humans that sensitized normal assay animals to the vasopressor effects of norepinephrine and an-giotensin II has been reported (8). The present study was conducted to determine if a factor exists in the serum of salt-induced hypertensive rats that would enhance the vasopressor activity of exoge-nously administered norepinephrine in normotensive bioassay animals.
Materials and methods. Development of experimental hypertension. Sixty-eight male rats, initially weighing 166 ± 29 g (SD), were quartered in a climate controlled room (25° ± 2± and 50-60% relative humidity) with 12 hr of light each day (6 am to 6 pm). Animals were divided into three groups of 20-24 animals and placed on diets consisting of Purina Lab Chow with NaCl added to make up 1.3, 5.6, and 8.4% of the ration by weight. 1
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