Tolerance and osmotic response to food deprivation and salt loading in the herbivorous non-drinking Moroccan Spiny-tailed lizard Uromastyx nigriventris (Sauria: Agamidae)

2021 ◽  
pp. 1-15
Author(s):  
Bendami Safaa ◽  
Znari Mohammed

Abstract Animals inhabiting arid environments use a variety of behavioural and physiological strategies to balance their water and salt budgets. We studied the effects of dehydration and salt loading on osmoregulatory capacities in a large herbivorous desert lizard, the Moroccan Spiny-tailed lizard Uromastyx nigriventris, the family Agamidae. These lizards select plants with a high K+ to Na+ ratio of 15 to 20, and like other herbivorous lizards, effectively eliminate the extra electrolyte load, mainly via a pair of active nasal salt glands, which exude the extra ions from blood. Here we present results of a series of laboratory experiments, which tested a five-week food and water deprivation and the excretory response of nasal salt glands, during a short period of five days, following salt loading by two separated injections of KCl or NaCl at a 5-day interval (4th and 9th days). During food-water deprivation, hypohydrated lizards lost 32% of their initial body mass with a substantial decrease of their Body Condition Index and the tail volume as an index of energy (fat and then potential metabolic water) storage. Plasma osmolality significantly increased by 20%. There were also significantly increased plasma sodium, chloride, and total protein concentrations. On the other hand, there was no significant decrease in the plasma glucose level. Most of the salt loaded lizards secreted far more K+ than Na+ via the nasal glands, even after NaCl loading. The K+/Na+ ratio decreased only after two to three repetitive NaCl injections but insufficient Na+ was eliminated. Two successive KCl injections were successfully eliminated, but daily natural average K+ administration induced progressive hyperkaliemia. These experimental data agreed with previous observations showing variations of plasma Na+ and K+ concentrations in free-living lizards. The nasal gland constitutes the main route of Cl− excretion but the Cl−/(Na+ + K+) ratio may vary according to observations in other herbivorous species.

1990 ◽  
Vol 68 (5) ◽  
pp. 568-574 ◽  
Author(s):  
Savio W. T. Cheng ◽  
Edward F. O'Connor ◽  
William G. North

We examined the effects of acute and chronic treatments with naloxone on release of vasopressin and oxytocin from the hypothalamoneurohypophyseal system (HNS) in conscious, chronically instrumented Long–Evans rats. Plasma concentrations of vasopressin-associated neurophysin and oxytocin-associated neurophysin were evaluated before and during an intravenous infusion of 18% saline at 100 μL∙kg−1 body weight∙min−1 for 60 min. Acute treatment with naloxone (2.75 μmol/kg, intravenous) did not measurably alter basal plasma osmolality or vasopressin-associated neurophysin concentration, but it caused a three-fold rise in basal plasma oxytocin-associated neurophysin concentration (16 ± 2 to 46 ± 3 fmol/mL, p < 0.005). Chronic treatment with naloxone (13.75 μmol/day, subcutaneous pellets) increased plasma osmolality (292 ± 1 to 300 ± 2 mosmol/kg H2O, p < 0.01) by day 5, but it had no measurable effects on basal vasopressin- or oxytocin-associated neurophysin concentration. There were also no significant differences in plasma sodium concentration (144.8 ± 1.1 vs. 142.2 ± 1.4 mequiv./L) under both conditions. Acute and chronic treatments with naloxone accompanied by salt loading produced a five- and four-fold decrease in the rates that plasma concentration of vasopressin-associated neurophysin changed with plasma osmolality, compared with untreated salt-loaded control rats. For oxytocin secretion from the HNS, both treatments accompanied by salt loading substantially decreased the threshold for changes in relation to plasma osmolality; the rise in plasma concentration of oxytocin-associated neurophysin was similar at all levels of hyperosmotic stimulation. A strongly correlated relationship between plasma oxytocin-associated neurophysin and plasma osmolality (r = 0.739) found for control animals became poorly correlated following treatments (acute, r = 0.173; chronic, r = −0.079). Our results suggest that in conscious rats, endogenous opioid peptides enhance the secretion of vasopressin from neurones of the HNS in response to hyperosmotic stimulation but inhibit both basal and stimulated release of oxytocin.Key words: naloxone, vasopressin, oxytocin, neurophysin, conscious rats.


1989 ◽  
Vol 257 (6) ◽  
pp. F1108-F1116 ◽  
Author(s):  
C. W. Heilig ◽  
M. E. Stromski ◽  
J. D. Blumenfeld ◽  
J. P. Lee ◽  
S. R. Gullans

Previous studies demonstrated an accumulation of “idiogenic osmoles” in the brain with chronic salt loading. Amino acids are known to constitute a portion of these solutes, but the balance of the solutes has yet to be fully characterized. In the present study, 1H-nuclear magnetic resonance (NMR) spectroscopy and biochemical assays of rat brain were used to identify and quantify changes in organic solutes in two different animal models of hypernatremia: hypertonic salt loading and water deprivation. Five days of salt loading increased plasma sodium concentration (PNa) to 165 meq/l and 3 days of water deprivation increased PNa to 151 meq/l, compared with 141 meq/l in controls. Amino acids, methylamines, and polyols were all significantly higher in salt-loaded animals compared with controls. Specifically, higher contents of glutamine (+65%), glutamate (+27%), myo-inositol (+36%), phosphocreatine + creatine (PCr + Cr) (32%), glycerophosphorylcholine (GPC) (+75%), and choline (+114%) were observed. Sorbitol and betaine, osmolytes known to accumulate in the hypertonic inner medulla, were present in low amounts in the brain and were unchanged with salt loading. In contrast to the results with salt loading, no accumulation of brain organic solutes was detected after 3 days of water deprivation. Based on these findings, we propose that amino acids, methylamines, and polyols function as osmoregulatory solutes in the brains of salt-loaded rats in a manner similar to that observed in other biological systems, whereas 3 days of water deprivation is an insufficient stimulus for their accumulation.


2019 ◽  
Vol 317 (3) ◽  
pp. F547-F559 ◽  
Author(s):  
Luciano D. Mendoza ◽  
Kelly A. Hyndman

The collecting duct (CD) concentrates the urine, thereby maintaining body water volume and plasma osmolality within a normal range. The endocrine hormone arginine vasopressin acts in the CD to increase water permeability via the vasopressin 2 receptor (V2R)-aquaporin (AQP) axis. Recent studies have suggested that autocrine factors may also contribute to the regulation of CD water permeability. Nitric oxide is produced predominantly by nitric oxide synthase 1 (NOS1) in the CD and acts as a diuretic during salt loading. The present study sought to determine whether CD NOS1 regulates diuresis during changes in hydration status. Male and female control and CD NOS1 knockout (CDNOS1KO) mice were hydrated (5% sucrose water), water deprived, or acutely challenged with the V2R agonist desmopressin. In male mice, water deprivation resulted in decreased urine flow and increased plasma osmolality, copeptin concentration, and kidney AQP2 abundance independent of CD NOS1. In female control mice, water deprivation reduced urine flow, increased plasma osmolality and copeptin, but did not significantly change total AQP2; however, there was increased basolateral AQP3 localization. Surprisingly, female CDNOS1KO mice while on the sucrose water presented with symptoms of dehydration. Fibroblast growth factor 21, an endocrine regulator of sweetness preference, was significantly higher in female CDNOS1KO mice, suggesting that this was reducing their drive to drink the sucrose water. With acute desmopressin challenge, female CDNOS1KO mice failed to appropriately concentrate their urine, resulting in higher plasma osmolality than controls. In conclusion, CD NOS1 plays only a minor role in urine-concentrating mechanisms.


1985 ◽  
Vol 248 (2) ◽  
pp. E155-E161
Author(s):  
S. W. Cheng ◽  
W. G. North

The responses of vasopressinergic neurons to acute salt loading and to graded hemorrhage were studied in rats under conscious and anesthetized conditions. Chronically cannulated rats were used in this study so that pre- and postanesthetic conditions could be studied in the same animals. Anesthesia induced by a combination of ketamine hydrochloride and pentobarbital sodium (Nembutal) did not cause a release of vasopressin-associated neurophysin (VP-RNP). In response to infusion of 18% saline, animals in the anesthetized state had significantly greater increases in plasma osmolality (Posmol) and plasma sodium concentration than animals in the conscious state. However, the rate of increase in plasma VP-RNP concentration ([VP-RNP]) as well as the relationship between [VP-RNP] and Posmol were not significantly different for the two states. Graded hemorrhage caused similar rates of increase in [VP-RNP] for animals under conscious and anesthetized conditions. These data suggest that anesthesia induced by ketamine plus pentobarbital sodium does not change the responsiveness of vasopressinergic neurons to acute salt loading and to graded hemorrhage.


1986 ◽  
Vol 251 (3) ◽  
pp. R560-R568 ◽  
Author(s):  
G. H. Metzler ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay

The time course and mechanism of the natriuresis that accompanies 24 h of water, but not food, deprivation were studied in eight chronically catheterized dogs. Dogs were fed a controlled diet containing 35 meq of sodium, 110 meq of potassium, and 107 ml of water at 9:00 A.M. every day (time 0), and urine and blood samples were taken at 0, 2, 4, 6, 8, 10, 12, 16, 20, and 24 h after feeding on 3 consecutive days: the control, dehydration, and recovery days. Twenty-four hours of water deprivation decreased body weight by 880 g, increased plasma sodium by 7.2 meq, and increased plasma osmolality by 22.5 mosmol/kg. Cumulative daily sodium excretion increased from 30.4 +/- 2.8 meq on the control day to 50.7 +/- 5.7 meq on the dehydration day (P less than 0.01) and resulted in significant negative sodium balance that developed during the last half of the dehydration day. Cumulative sodium excretion during the first half of the dehydration day was not different from the corresponding period of the control day. Cumulative potassium excretion also increased from 91.9 +/- 4.5 meq during the control day to 123.0 +/- 6.7 meq during the dehydration day (P less than 0.01). Significant and progressive increases in plasma vasopressin concentration and renin activity were observed during water deprivation, but plasma aldosterone did not change from control levels. Furthermore, there was no correlation between the rate of sodium excretion and plasma vasopressin or aldosterone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)


2014 ◽  
Vol 307 (2) ◽  
pp. R225-R236 ◽  
Author(s):  
Mitsuhiro Yoshimura ◽  
Takanori Matsuura ◽  
Junichi Ohkubo ◽  
Takashi Maruyama ◽  
Toru Ishikura ◽  
...  

Nesfatin-1/NucB2, an anorexigenic molecule, is expressed mainly in the hypothalamus, particularly in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). Nesfatin-1/NucB2 is also expressed in the subfornical organ (SFO). Because the SON and PVN are involved in body fluid regulation, nesfatin-1/NucB2 may be involved in dehydration-induced anorexia. To clarify the effects of endogenous nesfatin-1/NucB2, we studied changes in nesfatin-1/NucB2 mRNA levels in the SFO, SON, and PVN in adult male Wistar rats after exposure to osmotic stimuli by using in situ hybridization histochemistry. Significant increases in nesfatin-1/NucB2 mRNA levels, ∼2- to 3-fold compared with control, were observed in the SFO, SON, and PVN following water deprivation for 48 h, consumption of 2% NaCl hypertonic saline in drinking water for 5 days, and polyethylene glycol-induced hypovolemia. In addition, nesfatin-1/NucB2 expression was increased in response to water deprivation in a time-dependent manner. These changes in nesfatin-1/NucB2 mRNA expression were positively correlated with plasma sodium concentration, plasma osmolality, and total protein levels in all of the examined nuclei. Immunohistochemistry for nesfatin-1/NucB2 revealed that nesfatin-1/NucB2 protein levels were also increased after 48 h of dehydration and attenuated by 24 h of rehydration. Moreover, intracerebroventricular administration of nesfatin-1/NucB2-neutralizing antibody after 48 h of water deprivation resulted in a significant increase in food intake compared with administration of vehicle alone. These results suggested that nesfatin-1/NucB2 is a crucial peptide in dehydration-induced anorexia.


2004 ◽  
Vol 286 (3) ◽  
pp. E337-E346 ◽  
Author(s):  
Noriko Kondo ◽  
Hiroshi Arima ◽  
Ryouichi Banno ◽  
Shinobu Kuwahara ◽  
Ikuko Sato ◽  
...  

Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of water deprivation (WD) or 12 days of salt loading (SL). Rats were injected with isotonic or hypertonic saline, and plasma AVP levels and AVP heteronuclear (hn)RNA expression in the supraoptic and paraventricular nuclei, an indicator of gene transcription, were examined in relation to plasma osmolality in each group. Plasma AVP levels were correlated with plasma Na levels in all groups. Whereas the regression lines relating plasma AVP to Na were almost identical among control, WD, and SL groups, the thresholds of plasma Na for AVP release were significantly decreased only in the PEG group. AVP hnRNA levels were also correlated with plasma Na levels in control and PEG groups, and the thresholds were significantly decreased in the PEG group. In contrast, there was no significant correlation of AVP hnRNA and plasma Na levels in WD and SL groups. Thus it was demonstrated that acute and chronic reduction in plasma volume affected the osmoregulation of AVP release and gene transcription in different ways.


2015 ◽  
Vol 50 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michael A. McKenney ◽  
Kevin C. Miller ◽  
James E. Deal ◽  
Julie A. Garden-Robinson ◽  
Yeong S. Rhee

Context: Twenty-five percent of athletic trainers administer pickle juice (PJ) to treat cramping. Anecdotally, some clinicians provide multiple boluses of PJ during exercise but warn that repeated ingestion of PJ may cause hyperkalemia. To our knowledge, no researchers have examined the effect of ingesting multiple boluses of PJ on the same day or the effect of ingestion during exercise. Objective: To determine the short-term effects of ingesting a single bolus or multiple boluses of PJ on plasma variables and to characterize changes in plasma variables when individuals ingest PJ and resume exercise. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: Nine euhydrated men (age = 23 ± 4 years, height = 180.9 ± 5.8 cm, mass = 80.7 ± 13.8 kg, urine specific gravity = 1.009 ± 0.005). Intervention(s): On 3 days, participants rested for 30 minutes, and then a blood sample was collected. Participants ingested 0 or 1 bolus (1 mL·kg−1 body weight) of PJ, donned sweat suits, biked vigorously for 30 minutes (approximate temperature = 37°C, relative humidity = 18%), and had a blood sample collected. They either rested for 60 seconds (0- and 1-bolus conditions) or ingested a second 1 mL·kg−1 body weight bolus of PJ (2-bolus condition). They resumed exercise for another 35 minutes. A third blood sample was collected, and they exited the environmental chamber and rested for 60 minutes (approximate temperature = 21°C, relative humidity = 18%). Blood samples were collected at 30 and 60 minutes postexercise. Main Outcome Measure(s): Plasma sodium concentration, plasma potassium concentration, plasma osmolality, and changes in plasma volume. Results: The number of PJ boluses ingested did not affect plasma sodium concentration, plasma potassium concentration, plasma osmolality, or changes in plasma volume over time. The plasma sodium concentration, plasma potassium concentration, and plasma osmolality did not exceed 144.6 mEq·L−1 (144.6 mmol·L−1), 4.98 mEq·L−1 (4.98 mmol·L−1), and 289.5 mOsm·kg−1H2O, respectively, in any condition at any time. Conclusions: Ingesting up to 2 boluses of PJ and resuming exercise caused negligible changes in blood variables. Ingesting up to 2 boluses of PJ did not increase plasma sodium concentration or cause hyperkalemia.


2009 ◽  
Vol 204 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Akiko Katoh ◽  
Hiroaki Fujihara ◽  
Toyoaki Ohbuchi ◽  
Tatsushi Onaka ◽  
W Scott Young ◽  
...  

We have generated rats bearing an oxytocin (OXT)-enhanced cyan fluorescent protein (eCFP) fusion transgene designed from a murine construct previously shown to be faithfully expressed in transgenic mice. In situ hybridisation histochemistry revealed that the Oxt–eCfp fusion gene was expressed in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) in these rats. The fluorescence emanating from eCFP was observed only in the SON, the PVN, the internal layer of the median eminence and the posterior pituitary (PP). In in vitro preparations, freshly dissociated cells from the SON and axon terminals showed clear eCFP fluorescence. Immunohistochemistry for OXT and arginine vasopressin (AVP) revealed that the eCFP fluorescence co-localises with OXT immunofluorescence, but not with AVP immunofluorescence in the SON and the PVN. Although the expression levels of the Oxt–eCfp fusion gene in the SON and the PVN showed a wide range of variations in transgenic rats, eCFP fluorescence was markedly increased in the SON and the PVN, but decreased in the PP after chronic salt loading. The expression of the Oxt gene was significantly increased in the SON and the PVN after chronic salt loading in both non-transgenic and transgenic rats. Compared with wild-type animals, euhydrated and salt-loaded male and female transgenic rats showed no significant differences in plasma osmolality, sodium concentration and OXT and AVP levels, suggesting that the fusion gene expression did not disturb any physiological processes. These results suggest that our new transgenic rats are a valuable new tool to identify OXT-producing neurones and their terminals.


1992 ◽  
Vol 262 (2) ◽  
pp. R310-R317 ◽  
Author(s):  
M. Kadekaro ◽  
J. Y. Summy-Long ◽  
S. Freeman ◽  
J. S. Harris ◽  
M. L. Terrell ◽  
...  

Progressive water deprivation increased plasma osmolality, plasma Na+ concentration, and hematocrit in proportion to the severity of dehydration. With increases of 2% in plasma osmolality (24 h dehydration), glucose utilization increased in the supraoptic nuclei and tended to increase in the neural lobe. With further dehydration, glucose utilization also increased in the paraventricular nuclei. These increases were paralleled by depletion of vasopressin and oxytocin contents in the neural lobe and by the enhanced secretion of both hormones into plasma, with a predominant increase of vasopressin. These changes were proportional to the degree of dehydration. With progression of dehydration, decreases in intracellular and extracellular volumes accentuate. Reductions in extracellular volume result in increased angiotensin II (ANG II) formation. Accordingly, glucose utilization in the subfornical organ (SFO), a primary site of ANG II action, increased after 48 and 72 h of dehydration. The median preoptic nucleus, which receives direct inputs from the SFO, also increased glucose utilization at these times. Glucose utilization also increased in the organum vasculosum laminae terminalis, probably in response to the converging inputs from osmoreceptors, volume receptors, and ANG II receptors. Decreases in glucose utilization were observed in the caudal and rostral ventrolateral medulla, perhaps as compensatory responses to decreased extracellular volume to prevent fall in arterial blood pressure.


Sign in / Sign up

Export Citation Format

Share Document