Hypertension must still be reckoned with in the etiology of arteriosclerosis although the rôle that it was thought to play does not seem so important. Changes of blood pressure alone are not considered by many to be sufficient for the production of arteriosclerosis. This may play some part, but there are many other factors mostly unknown which determine in any case the production of arterial lesions. With every systole of the heart, blood is forced out into the arterial system against a certain amount of resistance represented by the tonicity of the capillary area, and the amount of cohesion between the viscous blood and the walls of arterioles. When a dilatation of the capillaries over any large area takes place, the blood pressure falls, provided there is no compensatory contraction in other areas to make up for the decreased resistance in the dilated vessels. The viscosity of the blood, as such, probably has very little effect on the resistance to the flow. With the systole of the heart there is a sudden dilatation of the arch of the aorta, and a wave of expansion follows, which is transmitted to the periphery and is lost only in the capillaries. The blood pressure is constantly changing. Physiologically there are relatively wide variations in the pressure in a perfectly normal individual. There are some persons who have hypotension, a blood pressure much below the normal. Such persons have usually small hearts, small aortas, and they seem to have but little resistance to disease. Many diseases, especially the prolonged fevers, diminish markedly the blood pressure. Whether the hypertension is the cause of the structural changes that are found in the walls of the vessels, or is the result of the diminished area of the arterial tree through which the same amount of blood has to be driven as before the vessel walls became narrowed, is still disputed. As has been stated, experimental evidence would tend to place the initial blame upon the poisons circulating in the blood, which first damage the vessel walls. The subsequent changes then produce thickening and inelasticity. Some think (Allbutt) that the hypertension is primary. There are cases seen clinically that lend support to this view and there is experimental evidence also (v. Chap. II). Not infrequently individuals in middle life begin to show increase of arterial blood pressure without discoverable cause. In such case it may be that there is slowly progressing chronic nephritis. The urine if examined only superficially in single specimens may not reveal any abnormalities. Careful functional examination by means of the newer tests may reveal functional deficiency. It must not be supposed that all cases of increasing hypertension are cases of chronic nephritis. The opinion has already been expressed (Chap. III) concerning this point. Experience has convinced me that the opinion expressed in former editions is not altogether correct. =Age=