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It is known that changes of blood volume are associated with changes of urine flow. Moderate bleeding not sufficient to result in a drop of arterial blood pressure leads to oliguria. Mild plethora as induced by small transfusions of plasma (1), isooncotic aibumin (2), whole blood (3), or washed red cells (4) leads to diuresis. A possible explanation of this phenomenon could be sought in a hypothetical volume regulatory mechanism using nervous elements in the vascular walls to sense "the fullness of the blood stream," which according to Peters (5) "may provoke the diuretic response on the part of the kidneys." It was hoped that, by giving due regard to the elastic properties of the circulatory system and hence to the distribution of induced volume changes, a study of the distribution of sensitive end-organs in the vascular bed might yield some hints as to the probable nature and location of a volume regulatory mechanism. While the arterial tree, due to its high volume elasticity coefficient, has to be ruled out as a potential reservoir, there is evidence that from the viewpoint of their pressure volume relations the pulmonary and venous circulation form an appropriate unit for such a function (6-8). A volume change could be measured most accurately if the whole system or one compartment of average or greater than average distensibility had stretch receptors intercalated in its walls. While little is known about stretch receptors in the peripheral veins, a variety of sensitive nervous end-organs similar to those in the carotid sinus have been found in the intrathoracic circulation, particularly in the walls of the venae cavae, the pulmonary vein and both auricles (9, 10). The complex physiology of the sensitive nervous endorgans in the thoracic viscera has recently been

THE EFFECT OF NEGATIVE PRESSURE BREATHING ON URINE FLOW