'Sodium sensitivity' in man

Increased cell membrane permeability to sodium is proposed as the initial event leading to high blood pressure in susceptible subjects when sodium intake is increased. All cells, including circulating cells, would be affected, but a key role for endothelial cells in the pathophysiology of the diastolic blood pressure elevation is proposed. Involvement of capillary endothelium could increase capillary permeability to proteins, and thereby would contribute to the altered fluid distribution on the high sodium diet which has been observed. If movement of fluid into the interstitium raised interstitial fluid pressure, venous capacitance would fall and right atrial pressure would rise. Several mechanisms would cause vascular smooth muscle tone to increase. Altered fluid distribution correlates with the rise in diastolic blood pressure from reduced sodium to high sodium diet, but arteriolar constriction would reduce capillary flow so altered fluid distribution occurs first. Arteriolar constriction could serve as a negative feedback to the raised atrial filling pressure by reducing raised capillary flow, which would decrease both altered fluid distribution and interstitial fluid pressure rise. Consequently, diastolic blood pressure would be chronically raised in 'sodium sensitive' subjects taking increased amounts of sodium in the diet. The relationship of the findings to "essential" hypertension and to premorbid cardiovascular sequelae, and the key role of capillary endothelium in the development of "essential" hypertension is discussed.