Renal sodium handling and sodium sensitivity

The pathophysiology of hypertension, which affects over 1 billion individuals worldwide, involves the integration of the actions of multiple organ systems, including the kidney. The kidney, which governs sodium excretion via several mechanisms including pressure natriuresis and the actions of renal sodium transporters, is central to long term blood pressure regulation and the salt sensitivity of blood pressure. The impact of renal sodium handling and the salt sensitivity of blood pressure in health and hypertension is a critical public health issue owing to the excess of dietary salt consumed globally and the significant percentage of the global population exhibiting salt sensitivity. This review highlights recent advances that have provided new insight into the renal handling of sodium and the salt sensitivity of blood pressure, with a focus on genetic, inflammatory, dietary, sympathetic nervous system and oxidative stress mechanisms that influence renal sodium excretion. Increased understanding of the multiple integrated mechanisms that regulate the renal handling of sodium and the salt sensitivity of blood pressure has the potential to identify novel therapeutic targets and refine dietary guidelines designed to treat and prevent hypertension.

Characteristics of Sodium Sensitivity in Korean Populations

Sodium sensitivity (SS) is a variable response of blood pressure (BP) to changes in sodium intake. The present study evaluated the existence and the characteristics of subjects with SS in Koreans. One hundred one subjects with (n = 31, 57.7 +/- 9.8 yr) or without hypertension (n = 70, 40.8 +/- 16.5 yr) were given a low-sodium dietary approache to stop hypertension (DASH) diet (LSD) for 7 days and a high-sodium DASH diet (HSD) for the following 7 days. The prevalence of SS in the present study population was 27.7% (17.6% in the non-hypertensive subjects and 51.6% in the hypertensive subjects). Analysis of the non-hypertensive subjects showed that systolic BP, diastolic BP, and mean arterial pressure at baseline and after HSD were higher in the subjects with SS than the subjects without SS, and there were no differences after LSD. In the hypertensive subjects, there was no difference in the BP at baseline and after HSD whether or not the subjects had SS. However, the systolic BP of hypertensive subjects with SS was lower than hypertensive subjects without SS after LSD. In the present study population, subjects with SS have distinctive BP features unlike to subjects without SS.