Hypodipsic hypernatremia with intact AVP response to non-osmotic stimuli induced by hypothalamic tumor: a case report.
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Anatomical lesions of hypothalamic area associated with hypodipsic hypernatremia have been reported only rarely. We report here a case of hypodipsic hypernatremia induced by a hypothalamic lesion. A 25-yr-old man, who had been treated with radiation for hypothalamic tumor 5-yr before, was admitted for evaluation of hypernatremia and hypokalemia. He never felt thirst despite the elevated plasma osmolality and usually refused to drink intentionally. Plasma arginine vasopressin (AVP) level was normal despite the severe hypernatremic hyperosmolar state and urine was not properly concentrated, while AVP secretion was rapidly induced by water deprivation and urine osmolality also progressively increased to the near maximum concentration range. All of these findings were consistent with an isolated defect in osmoregulation of thirst, which was considered as the cause of chronic hypernatremia in the patient without an absolute deficiency in AVP secretion. Hypokalemia could be induced by activation of the renin-angiotensin-aldosterone system as a result of volume depletion. However, inappropriately low values of plasma aldosterone levels despite high plasma renin activity could not induce symptomatic hypokalemia and metabolic alkalosis. The relatively low serum aldosterone levels compared with high plasma renin activity might result from hypernatremia. Hypernatremia and hypokalemia were gradually corrected by intentional water intake only. (+info)
Intact osmoregulatory centers in the preterm ovine fetus: Fos induction after an osmotic challenge.
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We previously demonstrated a functional systemic dipsogenic response in the near-term fetal sheep (128-130 days; 145 days = full-term) with swallowing activity stimulated in response to central and systemic hypertonic saline. Preterm fetal sheep (110-115 days) do not consistently demonstrate swallowing in response to hypertonic stimuli, and it is unclear whether this is due to immaturity of osmoreceptor mechanisms or neuronal pathways activating swallowing motor neurons. To determine whether osmoreceptive regions in the preterm fetus are activated by changes in plasma tonicity, we examined Fos expression with immunostaining in these neurons in response to an osmotic challenge. Nine preterm fetal sheep [five hypertonic saline-treated fetuses (Hyp) and four isotonic saline-treated fetuses (Iso)] were prepared with vascular and intraperitoneal catheters. Seventy-five minutes before tissue collection, hypertonic (1.5 M) or isotonic saline was infused (12 ml/kg) via an intraperitoneal catheter to fetuses. Brains were examined for patterns of neuronal activation (demonstrated by Fos protein expression). Hyp demonstrated increases in plasma osmolality (~10 mosmol/kg H(2)O) and Na concentrations (5 meq/l). Increased Fos expression was detected in Hyp in the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), median preoptic nucleus (MnPO), supraoptic (SON), and paraventricular nuclei (PVN) compared with Iso animals. Neuronal activation within the OVLT, SFO, and MnPO indicates intact osmoregulatory mechanisms, whereas activation of the SON and PVN suggests intact fetal neural pathways to arginine vasopressin neurons. These results suggest that preterm fetal swallowing insensitivity to osmotic stimuli may be due to immaturity of integrated motor neuron pathways. (+info)
Circulating relaxin acts on subfornical organ neurons to stimulate water drinking in the rat.
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Relaxin, a peptide hormone secreted by the corpus luteum during pregnancy, exerts actions on reproductive tissues such as the pubic symphysis, uterus, and cervix. It may also influence body fluid balance by actions on the brain to stimulate thirst and vasopressin secretion. We mapped the sites in the brain that are activated by i.v. infusion of a dipsogenic dose of relaxin (25 microg/h) by immunohistochemically detecting Fos expression. Relaxin administration resulted in increased Fos expression in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus, and magnocellular neurons in the supraoptic and paraventricular nuclei. Ablation of the SFO abolished relaxin-induced water drinking, but did not prevent increased Fos expression in the OVLT, supraoptic or paraventricular nuclei. Although ablation of the OVLT did not inhibit relaxin-induced drinking, it did cause a large reduction in Fos expression in the supraoptic nucleus and posterior magnocellular subdivision of the paraventricular nucleus. In vitro single-unit recording of electrical activity of neurons in isolated slices of the SFO showed that relaxin (10(-7) M) added to the perfusion medium caused marked and prolonged increase in neuronal activity. Most of these neurons also responded to 10(-7) M angiotensin II. The data indicate that blood-borne relaxin can directly stimulate neurons in the SFO to initiate water drinking. It is likely that circulating relaxin also stimulates neurons in the OVLT that influence vasopressin secretion. These two circumventricular organs that lack a blood-brain barrier may have regulatory influences on fluid balance during pregnancy in rats. (+info)
Energy balance, metabolism, hydration, and performance during strenuous hill walking: the effect of age.
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We aimed to examine the effect of age on energy balance, metabolism, hydration, and performance during 10 days of strenuous hill walking. Seventeen male subjects were divided into two groups according to their age. The nine subjects in group 1 constituted the younger group (age 24 +/- 3 yr), whereas eight older subjects were in group 2 (age 56 +/- 3 yr). Both groups completed 10 consecutive days of high-intensity hill walking. Mean (range) daily walking distances and ascent were 21 km (10-35 km) and 1,160 m (800-2,540 m), respectively. Energy intake was calculated from weighed food intake, and energy expenditure was measured by the doubly labeled water method. Blood and urine were sampled on alternative days to determine any changes in metabolism and hydration during the 10 days. Subjects also completed a battery of tests that included muscular strength (handgrip), jump performance, cognitive processing time, and flexibility. The younger group remained hydrated, whereas the older group became progressively dehydrated, indicated by a near twofold increase in urine osmolality concentration on day 11. This increased urine osmolality in the older group was highly correlated with impairment in vertical-jump performance (r = -0.86; P < 0.05) and decreased cognitive processing time (r = 0.79; P < 0.05). Despite energy expenditure of approximately 21 MJ/day, body mass was well maintained in both groups. Both groups displayed a marked increase in fat mobilization, reflected in significantly lowered prewalk insulin concentrations and elevated postwalk glycerol and nonesterified fatty acid concentrations. Despite the dehydration and impaired performance in the older group, blood glucose concentrations were well maintained in both groups, probably mediated via the increased mobilization of fat. (+info)
Some central mechanisms of thirst in the dog.
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Measurements of water intake were made on a population of trained conscious dogs of both sexes prepared with chronic third ventricle cannulae. 2. Injection of 100 ng angiotensin II into the third ventricle lead to a prompt stimulation of drinking, the mean water intake over a 5 min period being 503 +/- 89 ml. (n=6) compared with controls. This dipsogenic effect of angiotensin II was abolished by prior central administration of 10 mug saralasin acetate or 100 ng atropine. 3. Injection of 1 mug carbachol into the third ventricle produced a small, variable increase in drinking. 4. Injection of 0-2 ml. 5% NaCl into the third ventricle stimulated drinking, a response that was not affected by prior administration of 10 mug saralasin acetate or 100 ng atropine. 5. Following a 24 hr period of water deprivation there was an increase in plasma osmolality and plasma-renin activity. The drinking following this period of water deprivation was not affected by prior control administration of either 10 mug saralasin acetate or 100 ng atropine. 6. In two acute dogs, intracarotid infusion of 125I angiotensin II was not followed by significant appearance of radioactivity in the third ventricle or cisterna magna c.s.f. 7. The relevance of these results to the control of water intake is discussed. (+info)
Estrogen effects on osmotic regulation of AVP and fluid balance.
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To determine estrogen effects on osmotic regulation of arginine vasopressin (AVP) and body fluids, we suppressed endogenous estrogen and progesterone using the gonadotropin-releasing hormone (GnRH) analog leuprolide acetate (GnRHa). Subjects were assigned to one of two groups: 1) GnRHa alone, then GnRHa + estrogen (E, n = 9, 25 +/- 1 yr); 2) GnRHa alone, then GnRHa + estrogen with progesterone (E/P, n = 6, 26 +/- 3). During GnRHa alone and with hormone treatment, we compared AVP and body fluid regulatory responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml. min(-1). kg body wt(-1)), drinking (30 min, 15 ml/kg body wt), and recovery (60 min of seated rest). Plasma [E(2)] increased from 23.9 to 275.3 pg/ml with hormone treatments. Plasma [P(4)] increased from 0.6 to 5.7 ng/ml during E/P and was unchanged (0.4 to 0.6 ng/ml) during E. Compared with GnRHa alone, E reduced osmotic AVP release threshold (275 +/- 4 to 271 +/- 4 mosmol/kg, P < 0.05), and E/P reduced the AVP increase in response during HSI (6.0 +/- 1.3 to 4.2 +/- 0.6 pg/ml at the end of HSI), but free water clearance was unaffected in either group. Relative to GnRHa, pre-HSI plasma renin activity (PRA) was greater during E (0.8 +/- 0.1 vs. 1.2 +/- 0.2 ng ANG I. ml(-1). h(-1)) but not after HSI or recovery. PRA was greater than GnRHa during E/P at baseline (1.1 +/- 0.2 vs. 2.5 +/- 0.6) and after HSI (0.6 +/- 0.1 vs. 1.1 +/- 1.1) and recovery (0.5 +/- 0.1 vs. 1.3 +/- 0.2 ng ANG I. ml(-1). h(-1)). Baseline fractional excretion of sodium was unaffected by E or E/P but was attenuated by the end of recovery for both E (3.3 +/- 0.6 vs. 2.4 +/- 0.4%) and E/P (2.8 +/- 0.4 vs 1.7 +/- 0.4%, GnRHa alone and with hormone treatment, respectively). Fluid retention increased with both hormone treatments. Renal sensitivity to AVP may be lower during E due to intrarenal effects on water and sodium excretion. E/P increased sodium retention and renin-angiotensin-aldosterone stimulation. (+info)
Behaviour of rats exposed to trichloroethylene vapour.
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Rats were exposed to trichloroethylene (TCE) vapour for about five five-day weeks at concentrations from 100 to 1 000 ppm, and at 100 ppm for 12 1/2 weeks. The social behaviour of paired male rats was observed periodically in the home cage for five minutes after they had been exposed to TCE. The principal finding was a consistent reduction of up to 24% in the total acitivity. A single day's exposure to TCE was sufficient at the highest concentration. At 100 ppm, a similar decline in activity was significant after 1 1/2 weeks' exposure in one experiment and 8 1/2 weeks' in another. The decline in activity was fairly uniform and not usually because of specific reductions in particular kinds of behaviour. However, exploration of the cage and submission to, or escape from, the other rat were sometimes specifically reduced. In an 'exploration-thirst' test, rats were deprived of water overnight and placed on two or three occasions in a previously unfamiliar cage. Rats exposed to 100, 200, or 1 000 ppm TCE found water and began drinking sooner than their controls without altering the rate of movement about the cage. These results suggest lowered performance in a familiar situation where rats are usually very active and some loss of inhibitory control in an unfamiliar one. At the present threshold limit value, repeated exposure to TCE eventually had effects similar to those of one day's exposure to a higher concentration, but only after a widely variable delay. (+info)
Disturbance of motivated behavior in rats by epileptic afterdischarges.
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Nearly all epileptic seizures in patients are characterized by deranged consciousness. We started to study changes in motivated behavior (drinking in thirsty rats) as a possible analogue of compromised consciousness during and after epileptic seizures. Epileptic afterdischarges (ADs) were elicited by stimulation of the dorsal hippocampus and/or thalamus. Rats with implanted electrodes (deprived of water for 24 hours) were trained to lick water from a narrow tube. After pretraining ADs were elicited eight times in each animal and access to water was allowed during different phases of the AD. Stimulation did not affect licking if no AD was induced. If stimulation was successful, licking was stopped in nearly 70 % of stimulations and modified (biting the tube) in 30 %. Hippocampal ADs (characterized by serrated waves in the EEG and by an arrest of behavior with subsequent automatisms) completely blocked licking, signs of recovery appeared during the interval between the AD and recurrent AD and it progressed during recurrent ADs. Thalamic ADs abolished licking in 82% of cases and immediately after ADs normal licking reappeared in 49 % of these observations. Our results suggest that changes in motivated behavior might serve as an analogue of compromised human consciousness. (+info)