Central regulation of sodium appetite

Abstract

Sodium appetite, the behavioural drive to ingest salt, is stimulated by prolonged physiological sodium deficiency in many animal species. The same neural mechanisms that are responsible for sodium appetite in laboratory animals may influence human behaviour as well, with particular relevance to the dietary salt intake of patients with diseases such as heart failure, renal failure, liver failure and salt-sensitive hypertension. Since the original experimental work of Curt Richter in the 1930s, much has been learned about the regulation of salt-ingestive behaviour. Here, we review data from physiology, pharmacology, neuroanatomy and neurobehavioural investigations into the stimulatory and inhibitory signals that regulate sodium appetite. A rudimentary framework is proposed for the brain circuits that integrate peripheral information representing the need for sodium with neural signals for the gustatory detection of salt in order to drive a motivated ingestive response. Based on this model, areas of remaining uncertainty are highlighted where future information would allow a more detailed understanding of the neural circuitry responsible for sodium appetite.

Can Dietary Sodium Intake Be Modified by Public Policy?

“…An example of such activation and de-activation of critical neural pathways by variations in sodium intake in laboratory animals is portrayed in Figure 1, which is drawn from a previous publication from one of our laboratories (15). Findings reported by a number of other laboratories provide extensive, plausible evidence of a primary role for CNS regulation of sodium appetite (14).…”

“…The importance of angiotensin II, aldosterone, and other peripheral signals to these CNS circuits activating sodium appetite is consistent with an objective of maintaining optimal extracellular volume status (14).…”

“…That body of research began with the landmark experiments of Richter (13), which provided the first direct evidence that animals expressed an ingestive behavior designed to assure survival when threatened by sodium depletion. Decades of subsequent research worldwide, much of it published within the past 20 yr, has been summarized by one of the current authors (14). This work has revealed a complex neural network distributed among multiple centers in the brain, which integrates coordinated peripheral input from a number of organs via neural and hormonal signals.…”

Short-term sodium inputs attract microbi-detritivores and their predators

“…Low nutrient availability relative to the requirement of the organism forces organisms to spend more time acquiring these nutrients or suffer performance deficits (Arms et al, 1974;Sterner and Elser, 2002;Simpson et al, 2006;Geerling and Loewy, 2008). In this way, the stoichiometric imbalances between consumers and their food can affect the composition and ecological functions provided by food webs (White, 1993;Wardle, 2002).…”

“…This pattern is particularly apparent for the micronutrient sodium (Na). Plants require and concentrate very little Na in general, but heterotrophs need to concentrate Na well above plant levels to maintain neural function, osmotic balance, reproduction and development (Ganguli 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 et al., 1969;Bursey and Watson, 1983;Blumwald et al, 2000;Geerling and Loewy, 2008). Schowalter et al (1981) measured plant, herbivore, and predator Na concentrations at 0.02, 0.31, 0.66% Na respectively, which demonstrates the large stoichiometric disparity between plants and herbivores.…”