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Fifteen normal volunteers received one insulin injection or saline in two nonconsecutive days. At 0', 30', 60' and 90' water intake was measured. Simultaneously subjective thirst and hunger were recorded by running a set of psychological tests. Water intake was higher after insulin than saline at 60' and 90'. Insulin increases thirst sensation even before the sensation of hunger.
Angiotensin is a potent dipsogenic substance and causes elevated water intake in some pathological conditions but as yet no physiological role for angiotensin in normal thirst has been proven. If angiotensin is important in normal drinking, then it should contribute to the drinking which follows water deprivation. The rehydration of bilaterally nephrectomized rats, rats with bilateral ureteric ligation and control rats was compared after 21 hours of water deprivation. The total intake during the 6 hour rehydration was the same in the 3 groups despite the differences in the level of circulating angiotensin. Thus the renal renin-angiotensin system is not essential for deprivation-induced drinking. Another way to test any contribution to drinking by angiotensin is the administration of the competitive angiotensin inhibitor, saralasin acetate. In a control experiment saralasin acetate was found to block the dipsogenic effect of intravenous angiotensin. The infusion of saralasin acetate in a wide range of doses did not, however, affect the drinking following ligation of the inferior vena cava. Thus angiotensin is not essential for drinking following caval ligation. Two possible explanations for these results are that angiotensin is not normally involved in these types of thirst or that there is redundancy in the control of drinking with compensation for blocked mechanisms.
In male albino rats, bilateral lesions in the anterior zona incerta which decrease ad lib and food-deprivation water intake and osmotic thirst but leave hypovolemic thirst intact, severely impaired or abolished drinking in response to systemic injections of isoproterenol or central administration of angiotensin II. Water intake following water deprivation was reduced by one-fourth. Reasons for the dissociation of responses to hypovolemia, water deprivation, isoproterenol and angiotensin were suggested.
The role of endogenous brain angiotensin II (AII) in various thirst states was examined in the rat using the angiotensin converting enzyme inhibitor, captopril. Intracerebroventricular (ICV) captopril (7 micrograms) significantly attenuated the dipsogenic response to centrally administered angiotensin I (AI) (200 ng) for up to 2 hours. The same dose of captopril significantly potentiated the dipsogenic response to ICV AII (100 ng) but failed to alter the dipsogenic response to ICV carbachol (200 pmoles). Central pretreatment with captopril (7 micrograms), for 30 minutes, failed to alter markedly the cumulative water intake of 24 hour water deprived rats. However, a small, significant 8% decrease in water intake was noted in ICV captopril treated rats 60 minutes following the return of water. The same dose of captopril, administered intraperitoneally, significantly potentiated the cumulative water intake of 24 hour water deprived rats. Central pretreatment with captopril (7 micrograms), for 30 minutes, failed to alter the cumulative water intake of rats treated intraperitoneally with hypertonic saline (0.75 M given at a dose of 1% of the body weight). From these studies it would appear that central angiotensin converting enzyme plays only a minor role in thirst induced by water deprivation.
Male Sprague-Dawley rats were utilized to study the effects of the opioid receptor antagonists, naloxone and naltrexone, on thirst induced by thermal dehydration. In an initial experiment, the depressant effect of naloxone (1.0 mg/kg, IP) on the water intake of rats deprived of water for 24 h was confirmed. In subsequent experiments, rats were thermally dehydrated by exposing them without water to a 40 degrees C environment for 1-4 h. Following heat exposure, rats were injected with either naloxone or naltrexone either IP or ICV. Fifteen minutes later, rats were provided with water and water intake was measured for 2 h. Both naloxone and naltrexone had dose (0.1-5.0 mg/kg, IP)-dependent effects of reducing water intake of rats thermally dehydrated for 3 h. Water intake of rats thermally dehydrated for 2 or 4 h was also attenuated by pretreatment with naloxone. Rats thermally dehydrated for 3 h exhibited decreases in water intake following ICV injection of either naloxone or naltrexone at a dose of 50 micrograms. Neither naloxone nor naltrexone had an effect on urine output in any experiment. The water intake data support the hypothesis that thirst induced by thermal dehydration in rats is modulated by an opioid mechanism.
The present study examined whether thirsty rats pretreated with the dopamine receptor blocker, pimozide, would show patterns of unconditioned drinking behavior similar to those produced by reductions in water deprivation. An examination of the drinking behavior of 23-, 16-, 12-, 4-, and 0-h water-deprived animals showed that reductions in thirst produced increased latencies to initiate drinking, changes in the within-session pattern of licking, and reductions in the total number of licks emitted. In contrast, administration of pimozide to 23-h deprived rats produced no effect on either initiation latencies or lick patterns, and only marginally reduced the total number of licks emitted during the session. Finally, pimozide produced no effect on either individual lick durations or interlick intervals. These results suggest that the primary motivational (i.e., "thirst") mechanisms and motoric processes underlying drinking behavior are relatively invulnerable to pimozide challenge.
The classic " hypothalamocentric " theory of thirst has increasingly been challenged because the effects of hypothalamic lesions are not as behaviorally or anatomically specific as earlier research indicated. Instead, the attention of investigators in the field has increasingly been drawn to the lateral preoptic region and the tissues surrounding the anterior third ventricle. The present paper reviews these developments and proposes that still another diencephalic structure, the subthalamic region known as the zona incerta, may play a major role in the regulation of thirst and water intake.
This study investigated the role of brain angiotensin (Ang II) in thirst induced by hemorrhage. Hemorrhage by blood withdrawal from the femoral artery to 33% and 44% blood volume loss produces a dose response increase in plasma Ang II. In the brainstem there was no Ang II response to hemorrhage. In the hypothalamus, Brain Ang II was maximally elevated to 33% hemorrhage. Thus, plasma Ang II and brain Ang II had an independent response to hemorrhage. To further test the role of central versus peripheral Ang II, we tested the effect of central (50 mg) and peripheral (50 mg/kg) administration of captopril or central injection of 1 mg losartan or 3 mg CGP 42112A prior to a 33% hemorrhage in unanesthetized male Sprague-Dawley rats (250 g). Drinking was measured and AVP blood samples were taken before and after hemorrhage. The results show that central (i.v.t.) administration of captopril and losartan inhibited drinking compared to controls (0.33 +/- 0.3 ml vs. 2.3 +/- 0.8 ml: P < 0.05 and 0.20 +/- 0.09 ml vs.3.05 +/- 0.81 ml; P < 0.01, respectively) while peripheral (i.p.) captopril alone increased drinking in response to hemorrhage (5.81 +/- 0.81 ml vs. 2.3 +/- 0.8 ml; P < 0.05). AVP levels were elevated at 5 and 15 min, but neither injections of losartan or CGP 42112A i.v.t. affected this response to hemorrhage. We conclude that increased hypothalamic brain Ang II after hypovolemic hemorrhage stimulates thirst and blood pressure restoration and acts through AT1 receptors. The release of AVP in hemorrhage, however, does not rely exclusively on the angiotensinergic pathway in the brain.
Fifteen patients undergoing haemodialysis tasted soup varying in salt concentration and apple puree varying in sucrose concentration, immediately before and after dialysis. Matched controls tasted the same foods with a similar interval between tastings. The samples were rated for intensity, and on a relative-to-ideal scale. For the salt, the slopes of the functions plotted against log (concentration) were higher after dialysis than before, whilst the most preferred concentration was lower. There were no effects found for the sweetness ratings or for the controls. Likewise there were no overall differences in the ratings between the patients and controls. Thirst was found to increase on dialysis, and there was a trend of this being higher for the patients than for the controls. The reduction in preferences for salt by dialysis would make compliance with a reduced salt diet easier, but the increase in thirst would make compliance with reduced fluid intake more difficult.
Foods differ in their satiating effects; temperature and mode of presentation may be factors important for these differences. We tested the effects of these two variables in normal weight, non-dieting males and females using vegetable juice. The juice was offered as a preload, with females receiving 300 g and males receiving 400 g under conditions that systematically varied temperature (60-62 degrees C vs. 1 degrees C) and presentation (served in mug vs. bowl with spoon); a no-preload condition was also included. Each preload was followed within 5 min by a second course of grilled cheese sandwiches. In the males, intake was significantly lower after cold but not hot preloads in comparison to the no-preload condition; however, intakes following the hot and cold preloads did not differ significantly. Males also reported a significantly greater decline in thirst following the cold preloads. Temperature of the preloads did not affect food intake or thirst in the female subjects. Neither group was affected by the mode of presentation of the preloads. Further studies with other types of foods and drinks are needed to clarify whether temperature or mode of presentation can influence satiating efficiency.
In infant rats, kassinin exerts its antidipsogenic effect in the very early stages of neonatal life (2nd-3rd day). The inhibition of cell-dehydration drinking appears in rats of 2 days, and attains adult levels in pups of 9 days. Instead, the thirsts induced by suckling deprivation or by intracerebroventricular angiotensin II are inhibited by kassinin precociously (3rd day), but are unaffected by it in rats of 12-15 days. Kassinin also inhibits milk intake very early (3rd day) and this effect also disappears at 12 days of age. The pattern of ontogenetic results described here may be that of a brain kassinin-like tachykinin that, in the course of the development of the neural structures on which it acts, gains potent and selective control of cell-dehydration thirst.
A number of neuropeptides have been found to affect fluid intake when injected directly into the brain of various vertebrate species. These include: angiotensin II and its peptide precursors; the tachykinins Substance P, eledoisin and physalaemin; the opioid peptides met- and leu-enkephalin and beta-endorphin; bombesin; neurotensin; and vasopressin. Some of these stimulate drinking, some inhibit water intake, and the tachykinins have opposite effects on thirst depending on the species tested. Very little is known about the site or mechamism of action of most of these peptides or if their effects on thirst are physiological. The exception is angiotensin II, a peptide hormone that is synthesized in the blood in response to hypovalaemia or hypotension and is involved in many aspects of the regulation of blood volume and pressure. Angiotensin II injected intravenously or intracranially stimulates drinking in all reptiles, birds and mammals tested. In addition to its role as a hormone, angiotensin II may also function as a neurotransmitter or neuromodulator, since all of the enzymes and precursors necessary for its synthesis have been found in the central nervous system.
1. Subcutaneous (s.c.) administration of compound 48/80 elicited the increases of water intake, plasma beta-endorphin-like immunoreactivity, hypothalamic 3-methoxy-4-hydroxyphenylethyleneglycol sulfate and Hct in the rats. 2. The s.c. pretreatment of naloxone reduced the compound 48/80-induced water intake but had no effects on other variables. 3. Intracerebroventricular (i.c.v.) injection of naloxone attenuated the compound 48/80- and i.c.v. injected angiotensin II (ANG II)-induced water intake. 4. The hypothalamic norepinephrine metabolism was increased by s.c. injection of compound 48/80 but not by i.c.v. ANG II. 5. The present data suggest the possible involvement of opioid peptide (beta-endorphin) on the compound 48/80- and ANG II-induced thirst. However, it is uncertain whether hypothalamic norepinephrine is involved in the hypovolemic thirst mediated via stimulation of renin-angiotensin system.
Substantial progress has been made over the last 50 years in studies examining the neural and hormonal basis of thirst and salt appetite. We now understand much about the physiological systems that are engaged in response to perturbations of water and electrolyte balance, including the brain areas that are activated to elicit the appropriate behavioral responses as well as some of the neurotransmitters and hormones that are important in these behaviors. A brief summary of some of the critical and key findings associated with studies of thirst and salt appetite will be reviewed, followed by a discussion of three critical areas of research that have not been fully examined and represent viable future directions of this field.
OBJECTIVE: Intraperitoneal injection of a sialogogue, pilocarpine, at high concentrations induces salivation via peripheral pathways and thirst sensation via central pathways. In this study, we report that the effects of another sialagogue, cevimeline, on salivation and water intake in conscious rats differ from those of pilocarpine. DESIGN: We investigated that effects of peripherally and centrally injected cevimeline on parotid saliva flow rate and water intake in conscious rats. The results were compared with those of pilocarpine. RESULTS: The intraperitoneal injection of cevimeline induced salivation from the parotid gland, but not water intake. In contrast, the intracerebroventricular injection of cevimeline induced water intake without salivation. The concentration of cevimeline needed to induce salivation by intraperitoneal injection was several 10 times that of pilocarpine, but that needed to induce water intake by intracerebroventricular injection was over a 1000 times greater. CONCLUSIONS: The finding that intraperitoneally injected cevimeline induces salivation without inducing water intake, suggests that the effects on the thirst center in the brain are weaker than those of pilocarpine.
The current study examined the effects of intracerebroventricular (icv) infused aminopeptidase-resistant analogs of angiotensin II (AngII) and angiotensin III (AngIII) on thirst and sodium appetite. The analogs, [D-Asp1D-Arg2]AngII and [D-Arg1]AngIII, were further protected from degradation by pretreatment with the aminopeptidase A inhibitor, EC33, or the aminopeptidase N inhibitor, PC18. Prior to icv infusions, rats were sodium depleted with furosemide, followed by the angiotensin-converting enzyme inhibitor captopril, to block endogenous angiotensin formation. Both angiotensin analogs, at either of the two doses, were capable of eliciting fluid intakes of water and 0.3 M NaCl. Water and saline intakes were increased to a similar extent by 125 and 1250 pmol of [D-Asp1D-Arg2]AngII. [D-Arg1]AngIII produced a dose-dependent increase in water intake, whereas saline intake was equivalently increased by the 125 and 1250 pmol infusions. Pretreatment with EC33 or PC18 decreased water and saline intakes in response to [D-Asp1D-Arg2]AngII, while pretreatment with PC18 altered the time course of the [D-Arg1]AngIII-induced water and saline intakes. The ability of both inhibitors to decrease, but not completely block, AngII analog-induced intakes, coupled with the altered time course of the responses induced by the AngIII analog in the presence of PC18, supports the hypothesis that both AngII and AngIII are active ligands in brain angiotensin-mediated thirst and sodium appetite. However, these results do not resolve the primary question of whether conversion of AngII to AngIII is a prerequisite to dipsogenic and salt appetite responses in the brain.
Thirst and appetite-mediated ingestive behavior develop and are likely programmed in utero, thus preparing for newborn and adult ingestive behavior. Fetal swallowing activity is markedly different from that of the adult, as spontaneous fetal swallowing occurs at a markedly (six-fold) higher rate compared with spontaneous adult drinking activity. This high rate of fetal swallowing is critical for the regulation of amniotic fluid volume and the development of the fetal gastrointestinal tract. Disordered fetal swallowing has been associated with both a decrease (oligohydramnios) and increase (polyhydramnios) in amniotic fluid volume. Both conditions are associated with a significant increase in perinatal morbidity and mortality, and limited treatment modalities are currently available. The mechanisms underlying the high rate of human fetal swallowing are regulated, in part, by tonic activity of central angiotensin II, glutamate N-methyl-D-aspartate receptors, and neuronal nitric oxide synthase. Fetal hypertonicity-mediated dipsogenesis is likely programmed in utero, as offspring of water-restricted ewes demonstrate a programmed syndrome of plasma hypertonicity, with significant hematologic and cardiovascular alterations. Similar to dipsogenic mechanisms, peripheral and central fetal orexic mechanisms also develop in utero, as demonstrated by increased fetal swallowing after both oral sucrose infusion and central injection of neuropeptide Y. The role of leptin in regulating fetal ingestive behavior is interesting because, contrary to actions in adults, leptin does not suppress fetal ingestive behavior. Teleologically, this may be of value during the newborn period, as unopposed appetite stimulatory mechanisms may facilitate rapid fetal and newborn weight gain. An adverse intrauterine environment, with altered fetal orexic factors during the critical developmental period of fetal life, may alter the normal setpoints of appetitive behavior and potentially lead to programming of adulthood hyperphagia and obesity. Further research is needed to delineate the mechanistic relationship between the intrauterine environment and the development of the setpoints of adult appetite and thirst.
This paper reviews the experiments, which demonstrate conclusively the involvement of the abdominal vagus nerve in normal expression of most aspects of thirst in rats, by Gerard P. Smith and his colleagues published between 1975 and 1984. The nature of that vagal contribution differs with the type of primary thirst signal. Thus, there is no clear or unitary answer concerning whether the contribution of the vagus nerve is purely sensory, or some general tonic action within the central nervous system. Subsequent studies using cFos mapping of intracellular dehydration in conjunction with vagotomy and/or hepatic manipulations are also reviewed and further illustrate the involvement of abdominal information, both in the initiation as well as the termination of drinking. Many of the questions that were raised by Smith during these pioneering studies remain unaddressed and unanswered.