Osmoregulation is the term given to the control of WATER BALANCE in the body. It is a complex process involving the integrated actions of a variety of tissues, chemical processes, and of course behaviour. Animal bodies contain four fluid compartments: about two thirds of body water is contained within cells (INTRACELLULAR FLUID), the remaining one-third being outside cells (EXTRACELLULAR FLUID). There are three types of extracellular fluid: CEREBROSPINAL FLUID (which has relatively little to do with osmoregulation, forming only about 1% of the total body fluid volume); INTRAVASCULAR FLUIDS (that is, blood plasma; see BLOOD) which forms about 7.5% of the body fluid volume); and, making up the bulk of the extracellular fluids, INTERSTITIAL FLUID (the fluid found in the spaces between cells—about 25% of total body fluid volume). Intracellular, interstitial and intravascular fluids are separated by a SEMIPERMEABLE MEMBRANE: cell walls divide intracellular from interstitial fluids, and the walls of blood vessels separate intravascular fluids from all others. Interstitial fluids normally are ISOTONIC with the others so water remains in whatever compartment it is already in: if the interstitial fluids lose water (that is, become HYPERTONIC), fluid will be drawn out of cells (by a process of OSMOSIS). If the interstitial fluids become too diluted (that is, become HYPOTONIC), cells will gain water (again, by osmosis). The maintenance of an appropriate amount of water in the various body compartments uses two systems: osmometric thirst (the production of physiological changes and DRINKING following cellular dehydration) and VOLUMETRIC THIRST (which involves the production of physiological change and drinking following intravascular fluid maintenance).
Osmometric thirst. The KIDNEYS control the amount of water and SODIUM present in body fluids. NEPHRONS—a million or so individual functional units present in the kidney—take fluid from the blood and pass it to the ureter, which in turn connects to the bladder, from where excess fluid is released as urine. The volume of water retained or released by the kidney is under the control of the hormone VASOPRESSIN (which is also known as ANTIDIURETIC HORMONE). Vasopressin is synthesized in the PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS and the SUPRAOPTIC NUCLEUS. Neurons here are under complex neural control from a variety of different sites (see below under Neural mechanisms). Paraventricular and supraoptic neurons transport vasopressin along their axons to terminals in the posterior PITUITARY GLAND, where it is liberated into the blood stream. Vasopressin circulates in the blood and has an action on the kidney, causing water retention. Drinking too much water reduces vasopressin release; dehydration produces increased vasopressin release. Just as vasopressin acts on the kidney to preserve water; ALDOSTERONE (released from the ADRENAL GLAND) causes kidneys to retain sodium: if there is too much salt present in body fluids, aldosterone levels fall; if there is too little salt, aldosterone levels increase, to aid sodium retention.
Volumetric thirst. This is concerned with the control of blood volume. If blood volume is too high, increased blood pressure follows; if blood volume is too low (a state known as HYPOVOLAEMIA) cellular dysfunction and heart failure follow. Loss of blood is the commonest cause of hypovolaemia, but conditions such as vomiting and diarrhoea can also produce it. The kidneys are able to detect loss of blood flow: if this happens, kidney cells secrete a substance called RENIN into the blood. Renin is an ENZYME that converts ANGIOTENSINOGEN (which is present in the blood) to ANGIOTENSIN I (see ANGIOTENSIN). This is further converted by the enzyme ANGIOTENSIN CONVERTING ENZYME (ACE) to a highly active molecule, ANGIOTENSIN II which has an action on the brain, leading quickly to release of vasopressin, which in turn acts on the kidneys to prevent further water loss. Angiotensin II also has an action on the adrenal gland to stimulate aldosterone secretion, and stimulates contraction of blood vessels to increase blood pressure. In addition, angiotensin II is one of the most potent DIPSOGENS—chemicals that stimulate drinking—known to exist. Volumetric thirst is also stimulated by BARORECEPTORS in the heart: stretch receptors in the atria detect loss of blood volume when blood is returning to the heart after circulation. The atria also secrete atrial natriuretic peptide (ANP), which has a reverse action: baroreceptors work to detect hypovolaemia; ANP is released when there is too much water, working to inhibit secretion of renin, aldosterone and vasopressin, and to suppress drinking.
Neural mechanisms. There are three essential signals to brain that stimulate drinking. Volumetric thirst is signalled (1) via atrial baroreceptors (which transmit via the VAGUS NERVE to the NUCLEUS OF THE SOLITARY TRACT in the MEDULLA) and (2) by angiotensin II (which has an action on the AREA POSTREMA [which is intimately connected to the nucleus of the solitary tract] and SUBFORNICAL ORGAN, two CIRCUMVENTRICULAR ORGANS); osmometric thirst is be signaled by (3) OSMORECEPTORS. Osmoreceptors are neurons in the brain whose firing rate is affected by their level of hydration. Their precise location is still uncertain: osmoreceptors were not identified and named, but were predicted by theories of osmoregulation. It seems likely that the circumventricular organs (in this case the ORGANUM VASCULOSUM OF THE LAMINA TERMINALIS) are critically involved.
The subfornical organ, organum vasculosum of the lamina terminalis and nucleus of the solitary tract are all connected to the median preoptic nucleus. This in turn is connected to the paraventricular and supraoptic nuclei of the hypothalamus, which control vasopressin secretion. The nucleus of the solitary tract and preoptic areas are also connected to the lateral hypothalamus, which appears not to be involved in vasopressin regulation, but is involved in the initiation of drinking (see Clark et al., 1991). Clearly, this neural machinery is capable of responding independently to either osmometric or volumetric thirst, as it often must. It is quite conceivable to have for example, blood loss (due to wounding) without there being loss of fluid from the intracellular compartments. It is however also the case that both osmometric and volumetric thirst occur together (as happens when water is lost from the skin by evaporation). Brain processes involved in drinking—which are still not completely understood—are able to deal effectively with these various contingencies.
Clark J.M., Clark A.J.M., Warne D., Rugg E.L., Lightman S.L. & Winn P. (1991) Neuroendocrine and behavioural responses to hyperosmolality in rats with lesions of the lateral hypothalamus made by N-methyl-D-aspartate. Neuroscience 45:625–629.
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