oxytocin and Polyuria

Topics: Diabetes Insipidus; Endocrine System Diseases; Female; Humans; Kidney Diseases; Male; Neurophysins; Osmolar Concentration; Oxytocin; Pituitary Function Tests; Polyuria; Radioimmunoassay; Vasopressins

In the clinical setting, acute injuries in hypothalamic mediobasal regions, along with polydipsia and polyuria, have been observed in patients with cerebral salt wasting (CSW). CSW is also characterised by hypovolaemia and hyponatraemia as a result of an early increase in natriuretic peptide activity. Salt and additional amounts of fluid are the main treatment for this disorder. Similarly, experimental lesions to these brain regions, which include the median eminence (ME), produce a well-documented neurological model of polydipsia and polyuria in rats, which is preceded by an early sodium excretion of unknown cause. In the present study, oxytocin (OT) was used to increase the renal sodium loss and prolong the hydroelectrolyte abnormalities of ME-lesioned animals during the first few hours post-surgery. The objective was to determine whether OT-treated ME-lesioned animals increase their sodium appetite and water intake to restore the volume and composition of extracellular body fluid. Electrolytic lesion of the ME increased water intake, urinary volume and sodium excretion of food-deprived rats and also decreased urine osmolality and estimated plasma sodium concentration. OT administration at 8 hours post-surgery reduced water intake, urine output and plasma sodium concentration and also increased urine osmolality and urine sodium excretion between 8 and 24 hours post-lesion. From 24 to 30 hours, more water and hypertonic NaCl was consumed by OT-treated ME-lesioned rats than by physiological saline-treated-ME-lesioned animals. Food availability from 30 to 48 hours reduced the intake of hypertonic saline solution by ME/OT animals, which increased their water and food intake during this period. OT administration therefore appears to enhance the natriuretic effect of ME lesion, producing hydroelectrolyte changes that reduce the water intake of food-deprived animals. Conversely, the presence of hypertonic NaCl increases the fluid intake of these animals, possibly as a result of the plasma sodium depletion and hypovolaemic states previously generated. Finally, the subsequent increase in food intake by ME/OT animals reduces their need for hypertonic NaCl but not water, possibly in response to osmotic thirst. These results are discussed in relation to a possible transient activation of the ME with the consequent secretion of natriuretic peptides stored in terminal swellings, which would be augmented by OT administration. Electrolytic lesion of the ME may therefor

Topics: Animals; Appetite; Drinking; Eating; Male; Median Eminence; Natriuretic Agents; Oxytocin; Polyuria; Rats; Saline Solution, Hypertonic; Sodium; Water-Electrolyte Balance

This study analyzed the effects of systemic oxytocin (OT) administration and 48-h food deprivation on the polydipsia, hyperphagia, and polyuria produced by electrolytic lesions of the mediobasal hypothalamus (MBH). In a first experiment, food deprivation transiently decreased the polydipsic response, whereas food deprivation plus OT administration reduced the water intake and urine excretion of polydipsic animals but not their subsequent food intake. These results were replicated in a second experiment (20 days), which also showed that OT potentiates sodium excretion, reducing the estimated plasma sodium levels in food-deprived MBH-lesioned animals. Administration of OT on day 21 to food-deprived (from day 20 to 22) animals (second period of the experiment 2) blocked the differences in water intake and urine excretion volumes between MBH and control animals on days 21 and 22. Subsequently, this 48-h food deprivation induced an additional and lasting (days 23-40) reduction in the intake of water and food of MBH animals. According to these findings, OT administration and/or food deprivation may potentially exert enduring reducing effects on the polydipsia, polyuria, and hyperphagia of MBH syndrome.

Topics: Animals; Disease Models, Animal; Food Deprivation; Hyperphagia; Hypothalamus; Male; Oxytocin; Polydipsia; Polyuria; Rats; Rats, Wistar; Syndrome

We examined the effects of NaCl injections on the polydipsia and polyuria induced by subcutaneous oxytocin (OT) administration in food-deprived male rats. During the first 12 h of the treatment day, both food deprivation and OT administration increased urine excretion but reduced water intake, water balance (fluid intake minus urine volume) and body weight. OT treatment enhanced urine excretion and the reduction in water balance and body weight without reducing the water intake of food-deprived animals. Analysis of the physiological effects of OT administration showed increases in urinary sodium concentration, sodium excretion and a reduced plasma sodium concentration. During the second 12 h, OT increased both urine excretion and water intake in food-deprived but not in ad lib.-fed rats. However, hypertonic NaCl administration at the start of this second 12-h period blocked the polyuric and polydipsic responses observed in the OT/deprived group but increased the water intake of the ad lib. groups. After the whole 24-h period, animals treated with OT showed a water balance and body weight change matching those observed in Control animals. Although the recording time period is a critical factor to demonstrate the effect of peripheral OT administration on water intake, the results obtained suggest that the polyuric and polydipsic responses observed in food-deprived animals depend on the negative sodium and water balance induced by the natriuretic effect of OT and the unavailability of sodium. These OT-induced deficits can be counteracted by the administration of hypertonic NaCl solutions or simply by the intake of standard food.

Topics: Animals; Body Weight; Drinking; Drinking Behavior; Eating; Food Deprivation; Male; Oxytocin; Polyuria; Rats; Rats, Wistar; Sodium Chloride

Lesions of the tuberomammillary complex, a neuroanatomical system closely related to the hypothalamic supraoptic and paraventricular nuclei, induce strong polydipsia in male rats. It was recently demonstrated that this increase in water intake is immediate, persistent, follows circadian rhythms and appears to be related to sodium regulation. The present study found that urine osmolality was significantly lower in tuberomammillary-lesioned animals vs. their respective controls at 8:00 h after surgery. Therefore, the aim of the present study was to examine the natriuretic effect of intraperitoneal oxytocin (OT) administration on medial ventral tuberomammillary nucleus (E3) polydipsia and polyuria of lesioned and control male rats. At 24:00 h post-lesion, OT blocked the hyperdipsic and polyuric responses of E3-lesioned animals but not those of non-lesioned controls, which did however significantly increase their water intake. Moreover, urinary osmolality and sodium excretion increased in E3 -lesioned animals that received OT but not in lesioned controls receiving physiological saline (992 +/- 187.19 vs. 215.83 +/- 23.39 mOsm/kg; 1.68 +/- 0.13 vs. 0.47 +/- 0.1 mEq/L). At 48:00 h post-lesion, OT administration also induced a higher intake of water and of simultaneously offered hypertonic NaCl (1.5%) in E3-lesioned animals. These results are interpreted in terms of the hypothalamic systems involved in sodium and water homeostasis.

Topics: Animals; Drinking Behavior; Feeding Behavior; Hypothalamic Area, Lateral; Male; Osmolar Concentration; Oxytocin; Polyuria; Rats; Rats, Wistar; Sodium; Sodium Chloride; Time Factors; Urine; Water

Most mutations of the arginine vasopressin-neurophysin II (AVP-NPII) gene cause autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI). Such mutations are predicted to alter the three-dimensional structure of the prohormone, which accumulates in the cell body, ultimately leading to neuronal degeneration and hormonal deficit. In this study we describe the case of a 26-year-old female reporting a long-lasting history of polyuria/polydipsia. The father of the patient was affected by diabetes insipidus and was under desmopressin treatment until the time of his death. Nevertheless, the patient had never been subjected to endocrine evaluation.. Clinical and genetic studies were performed. An 8-h fluid deprivation test plus desmopressin challenge and a 5% saline solution test were performed, in order to confirm the diagnosis. DNA was extracted from peripheral blood lymphocytes and subjected to direct sequencing of the entire coding region of the AVP-NPII gene.. Clinical assessment of the patient confirmed the diagnosis of neurohypophyseal diabetes insipidus. Desmopressin treatment was started, which effectively reversed the polyuria/ polydipsia syndrome. Genetic analysis revealed a novel mutation (1665T>A) in exon 2 of the AVP-NPII gene, disrupting one of the disulfide bonds present in the NPII moiety which play a fundamental role in determining the proper folding of the molecule. In summary, in the present study we have described a novel mutation of the AVP-NPII gene, which is consistent with the malfolding/toxicity hypothesis underlying the pathogenesis of adFNDI.

Topics: Adult; Arginine Vasopressin; Base Sequence; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Drinking Behavior; Female; Humans; Molecular Structure; Mutation; Neurophysins; Oxytocin; Pedigree; Polyuria; Protein Precursors; Renal Agents

Vasopressin (AVP), angiotensin II (Ang II) and oxytocin (OT) receptors were mapped in the brain of inbred polydipsic mice of the STR/N strain by quantitative in vitro autoradiography and receptor binding levels, compared with those found in control non-polydipsic mice of the ICR strain. A remarkable difference was evidenced in the thalamic paraventricular nucleus where AVP receptor binding was 7- to 10-fold higher in polydipsic mice than in control mice. Another disparity was observed in the hypothalamic paraventricular nucleus, which contained AVP binding sites in the control mice, but was unlabelled in the polydipsic animals. Ang II receptor binding was reduced in the hypothalamic paraventricular nucleus of the polydipsic mice, whereas it was abundant in the brainstem region, encompassing area postrema and the nucleus of the solitary tract. The distribution and amount of OT receptor binding were similar in the polydipsic and control mice. Strain-related differences of AVP and Ang II receptor binding were observed both in male and female animals. A sex-related difference was seen only for OT receptor binding in the hypothalamic ventromedial nucleus, where labelling was less intense in males than in females of both strains. Altogether, our results support the view that central AVP and Ang II systems are involved in the mechanisms responsible for polydipsia in STR/N mice.

Topics: Angiotensin II; Animals; Drinking; Female; Iodine Radioisotopes; Male; Mice; Mice, Inbred ICR; Mice, Mutant Strains; Midline Thalamic Nuclei; Oxytocin; Paraventricular Hypothalamic Nucleus; Polyuria; Radioligand Assay; Receptors, Angiotensin; Receptors, Oxytocin; Receptors, Vasopressin; Sex Characteristics; Solitary Nucleus; Up-Regulation; Ventromedial Hypothalamic Nucleus

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Animals; Creatinine; Diuresis; Dogs; Glomerular Filtration Rate; Kidney; Lysine; Natriuresis; Oxytocin; Photometry; Pituitary Hormones, Posterior; Polyuria; Potassium; Time Factors; Urinary Catheterization; Vasopressins

Topics: Animals; Hypophysectomy; Kidney; Male; Natriuresis; Oxytocin; Pituitary Gland, Posterior; Polyuria; Rats; Water-Electrolyte Balance

Topics: Animals; Arginine; Chlorides; Ducks; Hypophysectomy; Kidney; Male; Oxytocin; Polyuria; Potassium; Sodium; Thirst; Time Factors; Urine; Vasopressins; Vasotocin