Arterial hypertension in the upper extremities has long been recognized as a frequent accompaniment of coarctation of the aorta (1), and has been produced experimentally by constriction of the aorta above the level of the origin of the main renal arteries in rats (2, 3) and in dogs (4,5,6,7).Pickering (8), studying the peripheral resistance in hypertension, and using a method which measured blood flow through heat elimination from the hand, examined three cases of coarctation. In these, as in all other examples of persistent hypertension which he studied, an abnormally high resistance to the flow of blood continued after influences from the nervous system had been released. Thus, pressor effects mediated through the nerves *ere excluded as a major cause of the increased peripheral resistance. Pickering believed that " a chemical abnormality of the blood " could be excluded also, because of the-differences in blood pressure readings between the upper and the lower extremities. He concluded, by exclusion of the factors mentioned, that the vascular narrowing in the upper limb was accounted for best by a local change in its vessels.The findings of other investigators are significant in relation to these conclusions. Lewis (9), and Blumgart, Lawrence and Ernstene (10) have shown that the blood supply is normal to both the upper and the lower extremities in patients with coarctation. Graybiel, Allen and White (11) found no evidence of muscular hypertrophy in the small arteries of the upper limb in coarctation.Prinzmetal and Wilson (12) also studied the effect of the release of vasoconstrictor nervous influences in hypertension by means of the plethysmograph. They measured blood flow through the forearm under conditions of increased temperature, and in some cases following the injection of novocain into the upper dorsal sympathetic ganglia. They concluded that the hypertension found in coarctation of the aorta was caused by a neurogenic increase in the peripheral vascular resistance. They were not in agreement with Pickering in this respect. For technical reasons, however, they did not attempt novocain injection into the dorsal sympathetic ganglia of patients with coarctation of the aorta.In the experimental animal, Goldblatt and his associates (4, 5) demonstrated that constriction of the abdominal aorta just above the origin of the main renal arteries had little or no immediate effect on the blood pressure above the site of the clamp; the immediate effect below the clamp was a lowering of blood pressure. In about 24 hours, however, it was observed that a hypertension developed above the site of the clamp. Further, it was found that with elevation of the carotid blood pressure there was a concomitant rise above normal in the femoral artery pressure, despite a substantial constriction of the aorta.Likewise, Steele (6) found that constriction of the aorta above the renal arteries in dogs resulted in hypertension both in the femoral and in the carotid arteries. He also found, by direct measurement, a definite diastolic ...

Experimental hypertension by the production of renal ischemia 1 suggests the possibility that the same abnormality underlies the mechanism of human hypertension. Smith and his associates 2 examined patients with essential hypertension by means of the diodrast clearance test3 and reported a reduction in the renal blood flow. However, Chesley and his associates,4 employing the same method of determining the renal blood flow, reported that the hypertension found in women suffering from toxemia of pregnancy was not associated with a reduction in renal blood flow, and they were not able Table 1.-Clearance Determinations in Normal Persons Patient A. Men 1. P. L.

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