1. A model system in dogs has been devised wherein major segmental infarction can be accomplished without surgical exposure and manipulation of the kidney. The model can be used to evaluate the effect of possible pharmacologic alteration of the infarction, as well as assess renal vein renin production after infarction. 2. Angiographic patterns of infarcts in dogs appear to duplicate those seen in patients, with the exception that staining due to a hyperemic infarct has not as yet been seen in the animal model. It would appear that collateral circulation develops rapidly after infarction both around and within the kidney. To recognize the true extent of the infarction, several projections of the selective renal artery injection should be taken, including lateral or steep oblique views. 3. The principal angiographic patterns which may be seen in infarction are: A. Radiolucent defects in the nephrogram during the acute or subacute phase of the infarction, secondary to obstruction of a segmental vessel. B. The "cortical palisade" effect due to blockage of multiple cortical interlobular arteries, with continued patency of others by atheromatous, blood clot, or fat emboli. A similar finding may be observed in segmental vessel blockage due to nonobstruction of an adjacent segment. C. Reduction in kidney size due to decreased blood flow. This may be seen on an acute or chronic basis, follow ing segmental artery obstruction. D. Local deformity of the renal outline, secondary to scarring of the infarct, with accompanying variation in contrast density in the nephrogram. E. Renal and perirenal collateral circulation, which can resemble tumor vascularity or vessels in an arteriovenous malformation. 4. In a limited survey of 7 animals, it would appear that renin production in the involved kidney can be increased following diffuse or segmental renal artery embolization. During the acute phase of infarction, a direct correlation of increased renal vein renin and elevated blood pressure was present in only 1 animal. There may be, however, a relationship between initial elevation of renin and increased blood pressure developing during the chronic phase of infarction. A definite correlation between elevated renin levels and the appearance or prominence of collateral circulation could not be made.