Overview of dietary sodium effects on and interactions with cardiovascular and neuroendocrine functions

The battle over salt has changed over the centuries from one of where to find salt sources to one of how much salt to use in a healthful manner. Many questions were answered by the INTERSALT Study across numerous countries and, yet, many questions persist. It is a love-hate relationship, an approach-avoidance paradigm. We need it but in excess it may cause harm. Questions that still remain are, Who is salt sensitive? What are the most appropriate and relevant models to study? What are the functional differences of the many salt effects? Can the data support a single public policy on dietary sodium recommendations? The following review examines some of these questions and the interaction of neural, neuroendocrine, renal, and social factors in the great salt debate. Dietary sodium can alter peripheral and central neurotransmitter concentrations, receptor density, and sensitivity. Low-sodium diets can produce acute neuroendocrine and neural compensations that are different from the chronic effects of low dietary sodium. Chronic high- or low-sodium diets may also cause trophic hormonal changes that can influence resistance vessel structure and, consequently, blood pressure. Both human and animal studies suggest a genetic basis for salt sensitivity. In some cases stress unmasks the salt sensitivity. For instance, the social context can modulate blood pressure responses to a high-sodium diet. Therefore, 24-h monitoring of blood pressure becomes important, especially in salt-sensitive persons.