2. The pressor material in ischemic renal perfusates originates directly in the kidney as a result of complete ischemia.

3. The pressor principle contained in ischemic renal perfusates is the cause of the hypertension which follows the reestablishment of circulation in completely ischemic kidneys, since perfusates of unreleased completely ischemic kidneys contain more pressor material than perfusates of released ischemic kidneys of the same animal.

4. The pressor principle in ischemic renal perfusates is presumed to be renin for the following reasons, (a) Both substances are destroyed by boiling, (b) Both substances induce tachyphylaxis. (c) The configuration of both pressor curves is identical, (d) The pressor action of both is not reversed by 933F, proving they are not epinephrine-like substances. (e) When incubated with plasma, both form a heat-stable pressor substance. (f) The pressor effect of both is uninfluenced by a previous injection of cocaine, (g) Unreleased, completely ischemic kidneys yield more pressor material on extraction than do released ischemic kidneys of the same animal.

5. The perfusates of blood-free ischemic kidneys contain more renin than those of blood-filled ischemic kidneys.

6. A method is described by which the power of various substances to inhibit or enhance the production of renin in the ischemic kidney may be tested.

7. A small amount of the heat-stable pressor substance, presumably angiotonin or hypertensin, is formed by the reaction of the pressor material (renin) and plasma in the vessels of the kidney during the period of complete ischemia.