Thirst and sodium appetite
Thirst and sodium appetite
The sensations caused by dehydration, the continuing loss of fluid through the skin and lungs and in the urine and feces while there is no water intake into the body. Thirst becomes more and more insistent as dehydration worsens. Water and electrolytes are needed to replace losses, and an adequate intake of sodium as well as water is important for maintaining blood volume. Normally, the amounts of water drunk and taken in food are more than enough to maintain hydration of the body, and the usual mixed diet provides all the electrolytes required.
Deficit-induced drinking occurs when a deficit of fluid in one or both of the major fluid compartments of the body serves as a signal to increase drinking. Cellular dehydration, detected by osmoreceptors, causes thirst and vasopressin release. Hypovolemia (low blood volume), detected by volume receptors in the heart and large veins and the arterial baroreceptors, causes immediate thirst, a delayed increase in sodium appetite, activation of the renin-angiotensin system, and increased mineralocorticoid and vasopressin secretion. Increases or decreases in amounts drunk in disease may result from normal or abnormal functioning of mechanisms of thirst or sodium appetite.
Observations using a variety of osmotic challenges have established that hyperosmotic solutions of solutes that are excluded from cells cause more drinking than equiosmolar amounts of solutes that penetrate cells. Thus, the osmotic shift of water out of the cells caused by the excluded solutes provides the critical stimulus to drinking. Continuing water loss in the absence of intake is perhaps a more significant cause of cellular dehydration than administration of an osmotic load, but the same mechanisms apply.
Sharing in the overall cellular dehydration are osmoreceptors which initiate the responses of thirst and renal conservation of water. Osmoreceptors are mainly located in the hypothalamus. The nervous tissue in the hypothalamus surrounding the anterior third cerebral ventricle and, in particular, the vascular organ of the lamina terminalis also respond to osmotic stimuli. Osmoreceptors initiating thirst work in conjunction with osmoreceptors initiating antidiuretic hormone (ADH) release to restore the cellular water to its prehydration level. In addition to reducing urine loss, ADH may lower the threshold to the onset of drinking in response to cellular dehydration and other thirst stimuli. The cellular dehydration system is very sensitive, responding to changes in effective osmolality of 1–2%.
The cells of the body are bathed by sodium-rich extracellular fluid that corresponds to the aquatic environment of the unicellular organism. Loss of sodium from the extracellular fluid is inevitably accompanied by loss of water, resulting in hypovolemia with thirst followed by a delayed increase in sodium appetite. If not corrected, continuing severe sodium loss eventually leads to circulatory collapse.
Stretch receptors in the walls of blood vessels entering and leaving the heart and in the heart itself are thought to initiate hypovolemic drinking. Volume receptors in the venoatrial junctions and receptors that register atrial and ventricular pressure respond to the underfilling of the circulation with a reduction in inhibitory nerve impulses to the thirst centers, which results in increased drinking. Angiotensin II and other hormones (such as aldosterone and ADH) are also involved in this response. Arterial baroreceptors function in much the same way as the volume receptors on the low-pressure side of the circulation, exerting continuous inhibitory tone on thirst neurons. A fall in blood pressure causes increased drinking, whereas an acute rise in blood pressure inhibits drinking. The anterior third cerebral ventricle region, which is implicated in angiotensin-induced drinking, plays a crucial role in hypovolemic drinking, body fluid homeostasis, and blood pressure control.
It is believed that drinking caused by hypovolemic stimuli partly depends on the kidneys. The renal thirst factor is the proteolytic enzyme renin, which is secreted into the circulation by the kidney in response to hypovolemia. Renin cleaves an inactive decapeptide, angiotensin I, from angiotensinogen, an α2-globulin that is synthesized in the liver and released into the circulation. Angiotensin I is converted to the physiologically active octapeptide angiotensin II during the passage of blood through the lungs. Angiotensin II is an exceptionally powerful stimulus of drinking behavior in many animals when administered systemically or into the brain. Increased activation of the renin-angiotensin system may sometimes account for pathologically increased thirst in humans. Angiotensin II also produces (1) a rise in arterial blood pressure, release of norepinephrine from sympathetic nerve endings, and secretion of adrenomedullary hormones; and (2) water and sodium retention by causing release of ADH from the posterior pituitary and stimulation of renal tubular transport of sodium through direct action on the kidney and indirectly through increased aldosterone secretion from the adrenal cortex. See Aldosterone, Kidney
Many substances released by neurons, and in some cases by neuroglial cells, affect drinking behavior when injected into the brain and may interact with the brain and modify angiotensin-induced drinking. Substances may stimulate or inhibit drinking, or both, depending on the species and the conditions of the experiment. Acetylcholine is a particularly powerful stimulus to drinking in rats, and no inhibitory effects on drinking have been described. Histamine also seems to be mainly stimulatory. However, a lengthening list of neuroactive substances, including norepinephrine, serotonin, nitric oxide, opioids, bombesin-like peptides, tachykinins, and neuropeptide Y, may either stimulate or inhibit drinking with varying degrees of effectiveness, depending on the species or the site of injection in the brain. Natriuretic peptides, prostaglandins, and gamma-amino butyric acid seem to be exclusively inhibitory. See Acetylcholine, Neurobiology, Synaptic transmission
Many hormones also affect water or sodium intake. Relaxin stimulates water intake, and ADH (or vasopressin) lowers the threshold to thirst in some species. Vasopressin injected into the third cerebral ventricle may stimulate water intake, suggesting a possible role for vasopressinergic neurons. Increased sodium appetite in pregnancy and lactation depends partly on the conjoint action of progesterone, estrogen, adrenocorticotrophic hormone (ACTH), cortisol, corticosterone, prolactin, and oxytocin. Aldosterone and other mineralocorticoids, the stress hormones of the hypothalamo-pituitary-adrenocortical axis, corticotrophin, ACTH, and the glucocorticoids also stimulate sodium intake. See Neurohypophysis hormone
The effect of many of these substances on drinking behavior shows both species and anatomical diversity. The multiplicity of effects of many of these substances makes it impossible to generalize on their role in natural thirst, but none of these substances seems to be as consistent and as universal a stimulus of increased thirst and sodium appetite as angiotensin.