Abstract
The arteriolar hypertonus responsible for hypertension is to be explained by one of the following mechanisms: 1. Increase in sympathetic vasoconstrictor impulses. 2. Circulating pressor substances. 3. A local disturbance in the vessels themselves.
The first factor has been ruled out since anesthetization of vasomotor nerves does not release the vascular hypertonicity. 1
That there is no increase in circulating pressor substances in the blood of patients with hypertension is indicated by the following experiments. Direct cross transfusions were performed between patients with malignant hypertension and subjects with normal cardiovascular systems (these subjects had inoperable carcinomata). Two Unger sets were employed simultaneously so that at no time was there an appreciable change in blood volume in either patient. Four such procedures were carried out, the amounts of blood interchanged being 500, 700, 1460 and 2000 cc. respectively. Congo red was injected into one subject before the transfusion. Forty-two percent of the dye was found in the blood of the other subject at the completion of the experiment.
If hypertension is due to a circulating pressor substance, a rise in blood pressure should be expected in the normal subjects with large amounts of hypertensive blood and a fall in pressure in the hypertensive patients with equivalent amounts of normal blood. No such changes were observed in either group.
Experimental hypertension was produced in dogs by the Goldblatt technique. 2 The tails of such dogs were then perfused alternately with their own heparinized or citrated arterial blood and with blood from normal dogs. A constant volume pump was used and the pressures required to force the blood through the tissues compared. In 4 instances the blood from the hypertensive dogs had a depressor effect and in one case a pressor effect as compared with blood from normal dogs.
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