Neuroendocrine regulation of salt and water metabolism

Abstract

Neurons which release atrial natriuretic peptide (ANPergic neurons) have their cell bodies in the paraventricular nucleus and in a region extending rostrally and ventrally to the anteroventral third ventricular (AV3V) region with axons which project to the median eminence and neural lobe of the pituitary gland. These neurons act to inhibit water and salt intake by blocking the action of angiotensin II. They also act, after their release into hypophyseal portal vessels, to inhibit stressinduced ACTH release, to augment prolactin release, and to inhibit the release of LHRH and growth hormone-releasing hormone. Stimulation of neurons in the AV3V region causes natriuresis and an increase in circulating ANP, whereas lesions in the AV3V region and caudally in the median eminence or neural lobe decrease resting ANP release and the response to blood volume expansion. The ANP neurons play a crucial role in blood volume expansion-induced release of ANP and natriuresis since this response can be blocked by intraventricular (3V) injection of antisera directed against the peptide. Blood volume expansion activates baroreceptor input via the carotid, aortic and renal baroreceptors, which provides stimulation of noradrenergic neurons in the locus coeruleus and possibly also serotonergic neurons in the raphe nuclei. These project to the hypothalamus to activate cholinergic neurons which then stimulate the ANPergic neurons. The ANP neurons stimulate the oxytocinergic neurons in the paraventricular and supraoptic nuclei to release oxytocin from the neural lobe which circulates to the atria to stimulate the release of ANP. ANP causes a rapid reduction in effective circulating blood volume by releasing cyclic GMP which dilates peripheral vessels and also acts within the heart to slow its rate and atrial force of contraction. The released ANP circulates to the kidney where it acts through cyclic GMP to produce natriuresis and a return to normal blood volume.

Effect of Brain Serotoninergic Stimulation on Sodium Appetite of Euthyroid and Hypothyroid Rats

“…The same authors also demonstrated that ANG II receptorcontaining neurons of the SFO project to the DRN (Tanaka et al 1998), which suggests that this pathway monitors circulating ANG II levels mediated by volume and/or sodium depletion. In summary, based on the above observations and evidence provided by Lind (1986), Johnson & Thunhorst (1997), McCann et al (1997), Fitch & Weiss (2000) and Franchini et al (2002), afferent information is conveyed to the NTS and from there to the DRN and ANG II-sensitive forebrain areas through pressure and/or volume receptors and renal sensors of tubular sodium load. At another level, increased circulating ANG II concentrations, reflecting body fluid volume and/or sodium depletion and a later increase in salt intake, are detected by the SFO, which conveys information to the DRN for the modulation of current sodium appetite.…”

The interrelationship between cholinergic pathway in the magnocellular paraventricular nucleus and natriuresis

“…CNS cholinergic stimulation contributed to the natriuretic effect, indicating the involvement of brain cholinergic system. Similarly, injection of carbachol into lateral ventricle, septal area, and preoptic region exerted the natriuresis and diuresis (Colombari et al 1992;McCann et al 1997).…”

Consequences of cerebroventricular insulin injection on renal sodium handling in rats: effect of inhibition of central nitric oxide synthase

“…It has been shown that many brain-specific natriuretic factors are located in periventricular structures related to water and salt balance control (3)(4)(5), demonstrating a possible link between insulin and natriuresis. Alternatively, we also cannot rule out the possibility that central NO-dependent neural pathways may control cholinergic, adrenergic or non-adrenergic non-cholinergic neurons and/or the hypothalamic/pituitary release of hormones, which in turn acutely modulates the action of insulin in the brain.…”

“…This observation has led to speculation that insulin may play a role in the development of increased blood pressure (1,2). On the other hand, the role of the central nervous system (CNS) in the control of blood pressure and hydroelectrolyte homeostasis has been demonstrated by several studies (3)(4)(5). Further studies of insulin action on neurons have demonstrated pleiotropic effects on ion flows (6), neurotransmitter uptake and release (7), cell growth, survival, and the transcriptional regulation of genes involved with differentiation (8), as well as possible modulation of several brain functions, such as food intake regulation, reproductive function and cardiovascular function (2,(9)(10)(11).…”