Search

Restricting dietary sodium promotes sodium appetite in rats. Prolonged sodium restriction increases plasma potassium (pK), and elevated pK is largely responsible for a concurrent increase in aldosterone, which helps promote sodium appetite. In addition to increasing aldosterone, we hypothesized that elevated potassium directly influences the brain to promote sodium appetite. To test this, we restricted dietary potassium in sodium‐deprived rats. Potassium restriction reduced pK and blunted the increase in aldosterone caused by sodium deprivation, but did not prevent sodium appetite or the activation of aldosterone‐sensitive HSD2 neurons. Conversely, supplementing potassium in sodium‐deprived rats increased pK and aldosterone, but did not increase sodium appetite or the activation of HSD2 neurons relative to potassium restriction. Supplementing potassium without sodium deprivation did not significantly increase aldosterone and HSD2 neuronal activation and only modestly increased saline intake. Overall, restricting dietary sodium activated the HSD2 neurons and promoted sodium appetite across a wide range of pK and aldosterone, and saline consumption inactivated the HSD2 neurons despite persistent hyperaldosteronism. In conclusion, elevated potassium is important for increasing aldosterone, but it is neither necessary nor sufficient for activating HSD2 neurons and increasing sodium appetite. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Salt intake is an established response to sodium deficiency, but the brain circuits that regulate this behavior remain poorly understood. We studied the activation of neurons in the nucleus of the solitary tract (NTS) and their efferent target nuclei in the pontine parabrachial complex (PB) in rats during sodium deprivation and after salt intake. After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-β-hydroxysteroid dehydrogenase type 2 (HSD2). In the PB, c-Fos labeling increased specifically within two sites that relay signals from the HSD2 neurons to the forebrain-the pre-locus coeruleus and the innermost region of the external lateral parabrachial nucleus. Then, 1-2 hours after sodium-deprived rats ingested salt (a hypertonic 3% solution of NaCl), c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, despite a large increase in c-Fos activation in the surrounding NTS (including the A2 noradrenergic neurons) and area postrema. Also after salt intake, c-Fos activation increased within pontine nuclei that relay gustatory (caudal medial PB) and viscerosensory (rostral lateral PB) information from the NTS to the forebrain. Thus, sodium deficiency and salt intake stimulate separate subpopulations of neurons in the NTS, which then transmit this information to the forebrain via largely separate relay nuclei in the PB complex. These findings offer new perspectives on the roles of sensory information from the brainstem in the regulation of sodium appetite. J. Comp. Neurol. 504:379-403, 2007. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

To reveal brainstem pathways activated by sodium deprivation and salt ingestion, nuclear c-Fos immunoreactivity (a marker for neuronal activity) was examined in neurons within the nucleus of the solitary tract (NTS) and in their efferent target nuclei within the pontine parabrachial complex (PB) in rats. After 8d dietary sodium deprivation, the aldosterone-sensitive neurons in the NTS, which express 11-13-hydroxysteroid dehydrogenase type 2 (HSD2), exhibited a marked increase in c-Fos immunoreactivity. In the PB, c-Fos labeling increased specifically within the two nuclei that relay information from the HSD2 neurons to the forebrain - the pre-locus coeruleus and the inner subdivision of the external lateral nucleus. In separate groups of rats that ingested salt (3% NaC1 solution) for 1 or 2h following 8d sodium-deprivation, c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, whereas a prominent increase in c-Fos labeling was found in the surrounding medial NTS (including A2 noradrenergic neurons) and area postrema. Salt ingestion also increased c-Fos labeling in PB nuclei that relay gustatory (caudal medial PB) and viscerosensory (rostral lateral PB) information from the NTS to the forebrain. Thus, sodium deficiency and salt ingestion stimulate separate subpopulations of neurons within the NTS, which transmit this information to the forebrain via largely separate nuclei in the PB. The existence of parallel, ascending signals for sodium need and salt intake offers a new perspective on the potential functions of brainstem sensory pathways in the regulation of sodium appetite. [ABSTRACT FROM AUTHOR]