Sodium, kidney, and circadian rhythm of blood pressure

Abstract

In healthy subjects, blood pressure falls during the night to 10%–20% less than that during the daytime. In some patients, such as those with hypertension and renal diseases, on the other hand, night-time blood pressure does not fall. This so-called nondipping phenomenon is tightly linked with high sodium sensitivity of blood pressure, microalbuminuria, and glomerular capillary hypertension. Interrelationships among these factors lead us to consider the important role of the kidney. I would like to propose that loss of renal functional reserve is the key to link these interrelationships. Loss of renal functional reserve, reduced ultrafiltration capacity, or enhanced tubular sodium reabsorption induces the sodium-sensitive type of hypertension. When sodium intake is high in patients with impaired renal function reserve, the defect in sodium excretory capability becomes evident, elevating blood pressure during the night (that is, nocturnal hypertension or nondipping) in order to compensate for diminished natriuresis during the daytime, causing enhanced pressure natriuresis during the night. Under such conditions, glomerular capillary pressure is also elevated dependent on systemic blood pressure, and increased albumin leakage into urine is its marker. When sodium intake is low, on the other hand, the defect remains latent, allowing blood pressure during the night to be lowered, that is dipping, as is seen in normal subjects.