THE NATURE OF THE COLD PRESSOR TEST AND ITS SIGNIFICANCE IN RELATION TO NEUROGENIC AND HUMORAL MECHANISMS IN HYPERTENSION 1

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Abstract
In each of 20 hypertensive patients, the cold pressor response was elicited in the usual manner and then repeated after the admn. of tetraethylammonium chloride (TEAC). One additional patient was tested in a similar manner 4 mo. after partial sympathectomy. In 8 cases, the response was again tested after high spinal anesthesia, and in 5 of these repeated as the anesthesia receded to lower levels. In 5 instances the effect of TEAC was again tested following the performance of the test under spinal anesthesia. Two phases of the blood pressure response to cold were noted. First, the response during the minute of exposure to cold (cold minute)[long dash]the classical cold pressor response, and 2d, delayed pressor responses after the hand had been removed from cold water. In all cases TEAC abolished the cold minute response, demonstrating that the effector phase of this reflex is neurogenic, and indicating that the cold pressor response may be useful in evaluating procedures designed to eliminate autonomic tone in hypertension. Release of varying portions of the arteriolar bed from active vasomotor control (by spinal anesthesia) produced dampening of the response which tended to vary directly with the extent of denerva-tion, but the smallest portion of the arteriolar bed which, under active vasomotor control, was capable of exciting clinically significant cold pressor reactivity varied from patient to patient. In one case with marked anxiety and resentment in response to the cold pressor test, there occurred following the cold minute exposure (during TEAC action) a very sharp transient rise in pressure. Similar, but less marked, delayed transient elevations were seen in eleven other patients. Since such a pressor response occurs at a time when autonomic impulses are blocked at the ganglia, it must be the result of a humoral agent (the action of such agents not being eliminated by TEAC). Six (30%) of the 20 patients failed to obtain a depressor effect from the admn. of TEAC, yet the cold pressor response was eliminated in each, suggesting that circulation of a humoral pressor agent, rather than failure of the drug to produce satisfactory autonomic blockade was responsible for the absence of depressor response in these patients. The data suggest that both humoral and neurogenic (autonomic) mechanisms may interact as clinically important factors in hypertension.