Abstract
The production of the acute malignant phase of experimental hypertension has been accomplished in seventeen dogs. The method used to produce this type of hypertension was the same as for the benign type (4), namely, constriction of the main renal arteries, or the equivalent, constriction of the aorta above the origin of both main renal arteries, but the constriction was especially severe. The malignant phase in the animals was characterized by hypertension, terminal renal insufficiency and the development of petechiae and larger hemorrhages in many internal organs, especially the alimentary tract. These were due to dissecting hemorrhage through, or rupture of, the wall of severely hyalinized or necrotic arterioles, or rupture of capillaries. Hyalinization and necrosis of arterioles were more severe and more widespread in animals that had a period of benign hypertension before the onset of renal insufficiency. In animals with a previous long period of benign hypertension, thickening of the media also occurred in arterioles, with or without hyalinized intima. Elevation of blood pressure (mechanical factor) and renal insufficiency (humoral factor) are at least two of the necessary conditions for the development of the necrotic arterioles and hemorrhages. Necrotic arterioles and hemorrhages have not yet been observed in animals that have had very high blood pressure for years without renal insufficiency, nor in animals with azotemia, due to removal of both kidneys, but without hypertension. Hyalinized retinal arterioles have been observed in dogs with persistent hypertension and with moderate or no disturbance of renal function. That ischemia is not the cause of the necrosis of the arterioles is shown by their absence from the ischemic kidneys of the dogs and their widespread presence in other organs that were not ischemic. These experiments show that the necrotic arterioles and hemorrhages are secondary to and not the primary cause of the malignant phase of hypertension.