Raab (1), in a study dealing with the effect of hyperventilation on the blood pressure of patients with arteriolar hypertension, concluded that there is a direct and constant relationship between the level of the blood pressure in patients with essential hypertension and the extent to which the CO2 tension of the arterial blood (alveolar CO2 tension) is lowered. The assumption was that hyperventilation produced lowering of the blood pressure in people with essential hypertension because of lowering of the CO2 content of the blood.1Previous to this work many physiologists had studied the effect of hyperventilation on people with normal arterial tension and in animals. Their methods differed so much from those of Raab and those presented here that comparisons are perhaps unjustifiable. Their results, however, are significant. Vincent and Cameron (2) in 1915 showed that hyperventilation in the human subject with normal blood pressure was associated with a rapid and considerable fall in blood pressure. This work confirmed earlier observations by Hill and Flack (3) and by Boothby (4). Collier, Densham, and Wells (5) found no effects of hyperventilation on the blood pressure of most of their human subjects with normal blood pressures. They thought that the systolic blood pressure was maintained nearly constant by means of a compensating cutaneous vasoconstriction. Schneider (6) agreed with this view. Vincent and Thompson (7) found that 37 out of 41 normal subjects showed a fall in blood pressure during a short period of hyperpnea. They suggested that the falls in blood pressure are due to mechanical interference with the return of blood to the heart, and that the lowered CO2 tension of the blood is only a subsidiary factor.In this study, an attempt has been made further to evaluate the significance of the CO2 factor in the blood in essential hypertension. Also in our subjects with hypertension, the effect of hyperventilation on the cardiac output, the pulse rate, and on the vital capacity of the lungs was observed.