CO₂ diuresis, with special reference to role of the left atrial stretch receptor mechanism

¹ Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire

CO₂ diuresis is probably mediated via a nonosmotic influence on the supraopticohypophyseal system. Since the left atrial stretch receptor mechanism is one such nonosmotic system which CO₂ might influence, experiments were designed to elucidate its role. It was found that CO₂ diuresis may be abolished by the erect posture or by applying tourniquets high on the thighs while supine, and that it may be restored by standing in a tank of water or by mild exercise. Increases in plasma volume, total blood volume, or pulmonary blood volume, which conceivably might stretch the left atrium, did not occur during CO₂ diuresis. Voluntary hyperventilation mimicking that which accompanies CO₂ inhalation resulted in a much smaller diuresis and one which, unlike that of CO₂, was accompanied by increased sodium excretion. Maintaining normal alveolar CO₂ tension during voluntary hyperventilation by simultaneous inhalation of 2% CO₂ in no way altered this result. Bilateral vagus section does not abolish CO₂ diuresis, but may enhance it. It is concluded, therefore, that the left atrial stretch receptor mechanism is not the afferent system for CO₂ diuresis.