Figure 1. Factors that influence arterial blood pressure. Blood pressure is proportional to cardiac output and the total peripheral resistance. The latter is dependent on the stiffness of the arterial walls and the level of arteriolar constriction. High intake of dietary salt causes a rise in extracellular (including plasma) osmolality during the postprandial phases. The elevation of extracellular osmolality results in an increase in the extracellular fluid (including blood) volume by various mechanisms: osmotic movement of cellular water to extracellular fluids, stimulation of the thirst center resulting in increased fluid intake, stimulation of renal salt excretion, and secretion of vasopressin that produces increased renal water retention. All of these mechanisms reduce the plasma salt level. The blood volume expansion increases cardiac output and induces arteriolar constriction (to prevent tissue overperfusion); both result in hypertension. The level of arteriolar constriction is regulated by the activities of vasoconstrictory (stretch, sympathetic activity, angiotensin II, epinephrine, vasopression, endothelin, etc.) and vasodilatory factors (acetylcholine, NO, etc.). Peripheral resistance increases with age mainly because the resistance vessels become thicker, stiffer, and narrowed due to arteriosclerosis (the replacement of the medial muscle fibers and intima by collagen) and atheromatosis (the deposition of lipids in vascular walls resulting in vascular inflammation and endothelial dysfunction). High salt also increases the blood pressure independent of blood volume expansion by direct effects on arterial smooth muscles, cardiac myocytes, hypothalamic control of blood pressure, and the local renin-angiotensin system. The blood pressure–raising effect of dietary salt increases with age mainly because of renal malfunction, which impairs salt excretion, and vascular alterations, such as arteriolar stiffening and decreased endothelial NO production. In addition, baseline plasma osmolality increases with age. The scheme shows the transition between an artery and an arteriole that controls tissue perfusion. In salt-resistant individuals, an increase in plasma osmolality induces a dilation of the artery (which prevents hypertension) while tissue perfusion remains constant due to arteriolar vasoconstrictory autoregulation. Age-related vessel stiffening impairs vessel dilation and contributes to the development of salt sensitivity of blood pressure.