Figure 1.

Extrinsic modulation of hydromineral balance (HB). The sketch shows that hyperosmotic stress modulates HB by the following approaches. (A) Activating the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT) and the medial preoptic nucleus (MnPO) in the anteroventral-third ventricle (AV3V) area, which in turn activates magnocellular cells. i.e., vasopressin (VP) and oxytocin (OT) neurons in the supraoptic (SON) and paraventricular (PVN) nuclei. (B) Changing activity of VP neurons after the osmolality is increased in brain parenchyma. (C) Causing retraction of astrocyte (Ast.) processes from the areas surrounding the osmosensory neurons, which increases the excitability of VP neurons by removing the physical barriers between adjacent neurons and by increasing extracellular levels of K⁺, glutamate (Glu) and angiotensin II (Ang II), and by reducing extracellular levels of atrial natriuretic peptide (ANP) or brain natriuretic peptide. (D) Resultant increases in intrahypothalamic release of OT can activate VP neurons through eliciting the retraction of astrocytic processes, while VP inhibits this retraction by increasing aquaporin expression. (E) In addition, hypovolemia or hypotension can increase VP release from the posterior pituitary (P.Pit) by reducing the baroreflex through the nucleus of the tractus solitarii (NTS) and by decreasing activity of the renin–angiotensin–aldosterone system (RAAS), while increasing the sympathetic output. As a result, serum osmotic pressure gets reduced and blood volume/pressure rises through increasing water reabsorption and natriuresis. See text for details.