The discussions of this article suggest that the pressure natriuresis mechanism of the kidneys is the most important of all long-term regulators of arterial pressure. This is especially so because of the infinite-gain feature of this mechanism, a feature that is explained here. However, experiments have shown that it is not the accumulation of sodium per se in the body that causes hypertension. Instead, it is the increase in extracellular fluid volume that usually accompanies sodium accumulation that increases the arterial pressure. If the increase in fluid volume is prevented, hypertension will not occur despite marked sodium retention. Long-term autoregulation in hypertension plays a very important role for two major reasons: (a) it greatly increases the total peripheral resistance when the cardiac output increases only a small amount, and (b) when it promotes arteriolar constriction, capillary pressure is reduced, which in turns allows a very large proportion of the extracellular fluid to remain in the blood rather than to leak into the interstitium. Marked loss of renal mass usually does not cause hypertension because, as long as there is a proper balance between glomerular filtration capability and tubular reabsorption capability, as little as 10% of the normal kidney mass theoretically can excrete the normal daily load of salt without a significant rise in arterial pressure. However, whenever the ratio of glomerular filtration capability to tubular reabsorption capability falls below normal, salt and water are retained until enough hypertension develops to overcome the deficit in glomerular filtration.