THOUGH ocular hypertension is one of the fundamental symptoms of glaucoma, we have as yet little clinical evidence for an evaluation of its pathological significance and real severity. The only elements at our disposal are those inferred by the study of the pressure curve both spontaneous and after miotic drugs. These studies show that at the onset of the disease the basic pressure may still be normal, in spite of a certain degree of instability; during the course of the disease the tension rises with diurnal phasic variations of wide range; in the late stages of the disease these diurnal variations become smaller and the basic pressure rises to a very high level. Leydhecker (1952) recently employed the usual provocative tests (waterdrinking, lability, mydriasis) to define the changes responsible for this symptom and evaluate its severity. His attempts led to uncertain conclusions, because our knowledge of the function primarily impaired, and of the exact mechanism of the tests employed is uncertain. In fact, the possibility of solving this problem depends upon the exact knowledge of the pathogenesis of hypertension as well as of the mechanism of action of the tests employed. With regard to the pathogenesis of the symptom, our views are confined to-day to two hypotheses which may be considered complementary. The first, elaborating the old conception of Priestley Smith (1879, 1891), maintains that hypertension is caused by an anatomical obstacle to the outflow of the aqueous. This obstacle is to be sought, according to Ascher (1949), in the aqueous veins, and, according to Goldmann (1948), in the trabeculae of the anterior chamber. An anatomical obliteration in the anterior aqueous drainage channels would, however, lead to a blocking of circulation, which makes it hard to explain the clinical behaviour of intra-ocular pressure. A mechanical obstacle present at a certain hour of the day cannot possibly be absent at another hour of the same day, when tension falls (DukeElder, 1952). Thomassen (1948) suggests a functional hindrance to the aqueous outflow caused by increased pressure in the episcleral venous vessels, into which the aqueous flows. A second hypothesis put forward by one of us (Cristini, 1951a) postulates the vascular nature of hypertension. It would result from a rise in the hydrostatic pressures in the uveal capillary-