Neural mechanisms in body fluid homeostasis.
Under steady-state conditions, urinary sodium excretion matches dietary sodium intake. Because extracellular fluid osmolality is tightly regulated, the quantity of sodium in the extracellular fluid determines the volume of this compartment. The left atrial volume receptor mechanism is an example of a neural mechanism of volume regulation. The left atrial mechanoreceptor, which functions as a sensor in the low-pressure vascular system, is located in the left atrial wall, which has a well-defined compliance relating intravascular volume to filling pressure. The left atrial mechanoreceptor responds to changes in wall left atrial tension by discharging into afferent vagal fibers. These fibers have suitable central nervous system representation whose related efferent neurohumoral mechanisms regulate thirst, renal excretion of water and sodium, and redistribution of the extracellular fluid volume. Efferent renal sympathetic nerve activity undergoes appropriate changes to facilitate renal sodium excretion during sodium surfeit and to facilitate renal sodium conservation during sodium deficit. By interacting with other important determinants of renal sodium excretion (e.g., renal arterial pressure), changes in efferent renal sympathetic nerve activity can significantly modulate the final renal sodium excretion response with important consequences in pathophysiological states (e.g., hypertension, edema-forming states).
D000344:Afferent Pathways / Q000502:physiology*; D000818:Animals; D001810:Blood Volume; D001826:Body Fluids / Q000502:physiology*; D004525:Efferent Pathways / Q000502:physiology*; D005110:Extracellular Space / Q000502:physiology; D006325:Heart Atria / Q000294:innervation; D006706:Homeostasis; D006801:Humans; D007668:Kidney / Q000294:innervation; D008465:Mechanoreceptors / Q000502:physiology; D009318:Natriuresis