The effect of water deprivation on signalling molecules that utilise cGMP in the spinifex hopping mouse Notomys alexis.

2004 ◽  
Vol 26 (2) ◽  
pp. 191 ◽  
Author(s):  
RA Heimeier ◽  
RC Bartolo ◽  
JA Donald
Keyword(s):  
Water Conservation ◽  
Water Deprivation ◽  
Free Water ◽  
Distal Colon ◽  
Proximal Colon ◽  
Mrna Levels ◽  
Physiological Mechanisms ◽  
Water Excretion ◽  
Signalling Molecules

In mammals the natriuretic and guanylin peptides influence renal and intestinal fluid content and electrolyte transport by binding to and activating guanylyl cyclase (GC) receptors that in turn stimulate production of the intracellular second messenger guanosine 3?:5?-cyclic monophospate (cGMP). However, the role of natriuretic and guanylin peptides in desert mammals is not understood. The spinifex hopping-mouse (Notomys alexis), has a suite of behavioural and physiological mechanisms that permits survival for extended periods without access to free water. Because signalling molecules that generate cGMP are known to promote water excretion, it was predicted that natriuretic and guanylin peptide synthesis would be down regulated in water-deprived N. alexis, and thus reduce the amount of water lost in the urine and faeces. However, in the kidney ANP and GC-A mRNA levels were increased in water-deprived mice, but CNP and GC-B mRNA levels were decreased. Water deprivation increased guanylin and uroguanylin mRNA expression in the distal colon, but it remained unchanged in the kidney and proximal colon. The expression of GC-C mRNA increased in the proximal colon but not in the distal colon. This study shows that water deprivation differentially affects the expression of regulatory molecules that stimulate cGMP production, and that a down-regulation associated with water conservation does not uniformly occur.

scholarly journals Intensive Care Unit Acquired Hypernatremia after Major Surgery is Associated with Urine Concentrating Defect: An Observational Study

2020 ◽  
Author(s):  
Philipp Deetjen ◽  
Ulrich Jaschinski ◽  
Axel Heller
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Water Balance ◽  
Water Conservation ◽  
Sodium Excretion ◽  
Free Water ◽  
Major Surgery ◽  
Surgical Intensive Care Unit ◽  
Surgical Intensive Care ◽  
Water Excretion

Abstract Background: Although intensive care acquired hypernatremia is a common event, limited knowledge exists about the pathogenesis of this disorder. The present study attempts to show that patients undergoing major surgery develop hypernatremia in the presence of both high salt and volume load and concentration disorder of the kidney with insufficient sodium excretion.Methods: In a retrospective study, all patients who were admitted to a 40-bed tertiary surgical intensive care unit of a university hospital from July 2019 to December 2019 with major surgery were examined. Hypernatremia was defined as a sodium value exceeding 145 mmol/l. In addition to the analysis of all patients, complete water and salt balances were performed in a smaller subgroup with 142 patients.Results: 23.9% of patients undergoing major surgery developed hypernatremia, whereby hypernatremia was associated with increased mortality. Patients with hypernatremia showed a renal concentration defect with decreased urine sodium concentration (65 (IQR: 44.8-90) mmol/l vs 78 (IQR: 46-107) mmol/l, p = 0.007) and decreased urine osmolality (514 (IQR: 465-605) mmol/l vs 602 (IQR: 467-740) mmol/l, p < 0.001). In the subgroup of patients with complete sodium and water balance, a positive salt and water balance was observed. After propensity score matching, we found a significantly increased electrolyte free water clearance (1020 ±1740 ml vs -560 ±1620 ml, p <0.001) in the hypernatremia group, together with an inadequately lower total sodium urine excretion (401 ±303 mmol vs 593 ±400 mmol, p = 0.02). Conclusion: The present study shows that postoperative hypernatremia is associated with an imbalance between perioperative salt and water load and renal sodium and water handling with inadequately low renal sodium excretion and inadequately high renal water excretion. The underlying renal concentration disorder may be explained by a defect in a natriuretic-ureotelic response a recently described renal urea-mediated water conservation mechanism after salt exposure.

Disorders of Water Balance

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress
Keyword(s):  
Water Balance ◽  
Water Intake ◽  
Serum Sodium ◽  
Water Conservation ◽  
Free Water ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Water Losses ◽  
Water Excretion ◽  
Impaired Water

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.

scholarly journals Diurnal variations in the concentrations of volatile fatty acids in the alimentary tracts of wild rabbits

1972 ◽  
Vol 27 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Susan J. Henning ◽  
F. J. R. Hird
Keyword(s):  
Fatty Acids ◽  
Volatile Fatty Acids ◽  
Distal Colon ◽  
Proximal Colon ◽  
Diurnal Variations ◽  
Gut Contents ◽  
Excretion Pattern ◽  
Colon And Rectum ◽  
High Concentrations

1. Wild rabbits were caught during both phases of the excretory cycle and their gut contents were analysed for volatile fatty acids (VFA).2. All rabbits were found to have high concentrations of VFA in the caecum and in the proximal colon. Acetic was the most abundant acid followed by n-butyric, then propionic.3. VFA concentrations in the caecum and in the proximal colon of rabbits caught during the day and during the night were similar. Hard pellets from the distal colon and rectum of rabbits caught during the night had considerably less VFA than did the soft pellets from rabbits caught during the day.4. Owing to the ingestion of soft faeces, the VFA content of stomach material was greater in rabbits caught during the day than in those caught at night.5. The results are discussed in terms of the mechanism of the diurnal excretion pattern and the role of coprophagy in the rabbit.

Alterations in Muc2 biosynthesis and secretion during dextran sulfate sodium-induced colitis

2002 ◽  
Vol 282 (2) ◽  
pp. G382-G389 ◽  
Author(s):  
Ingrid B. Renes ◽  
Jos A. Boshuizen ◽  
Daniëlle J. P. M. Van Nispen ◽  
Nathalie P. Bulsing ◽  
Hans A. Büller ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Cell Loss ◽  
Distal Colon ◽  
Proximal Colon ◽  
Histological Evaluation ◽  
Mrna Levels ◽  
Precursor Synthesis ◽  
Regenerative Phase ◽  
Active Disease

To gain insight into mucin 2 (Muc2) synthesis and secretion during dextran sulfate sodium (DSS)-induced colitis, rats were treated with DSS for 7 days. Colonic segments were excised on days 0 (control), 2 (onset of disease), 7 (active disease), and 14(regenerative phase) for histological evaluation. Explants were metabolically labeled with 35S-labeled amino acids or [35S]sulfate followed by chase incubation. Homogenates were analyzed by SDS-PAGE and 35S-labeled Muc2 was quantified. Also, total Muc2 protein and mRNA were quantified. DSS-induced crypt loss, ulcerations, and concomitant goblet cell loss were most pronounced in the distal colon. Muc2 precursor synthesis increased progressively in the proximal colon but was unaltered in the distal colon during onset and active disease. During the regenerative phase, Muc2 precursor synthesis levels normalized in the proximal colon but increased in the distal colon. Total Muc2 levels paralleled the changes seen in Muc2 precursor synthesis levels. During each disease phase, total Muc2 secretion was unaltered in the proximal and distal colon. [35S]sulfate incorporation into Muc2 only decreased in the proximal colon during active disease and the regenerative phase, whereas secretion of [35S]sulfate-labeled Muc2 increased. During the regenerative phase, Muc2 mRNA levels were downregulated in both colonic segments. In conclusion, DSS-induced loss of goblet cells was accompanied by an increase or maintenance of Muc2 precursor synthesis, total Muc2 levels, and Muc2 secretion. In the proximal colon, Muc2 became undersulfated, whereas sulfated Muc2 was preferentially secreted. Collectively, these data suggest specific adaptations of the mucus layer to maintain the protective capacities during DSS-induced colitis.

scholarly journals Nodal signalling in Xenopus : the role of Xnr5 in left/right asymmetry and heart development

Open Biology ◽  
2016 ◽  
Vol 6 (8) ◽  
pp. 150187 ◽  
Author(s):  
Emmanuel Tadjuidje ◽  
Matthew Kofron ◽  
Adnan Mir ◽  
Christopher Wylie ◽  
Janet Heasman ◽  
...  
Keyword(s):  
Heart Development ◽  
Cardiac Troponin ◽  
Axis Formation ◽  
Mrna Levels ◽  
Blastula Stage ◽  
Signalling Molecules ◽  
Tailbud Stage ◽  
Heart Field ◽  
Left Right Asymmetry

Nodal class TGF-β signalling molecules play essential roles in establishing the vertebrate body plan. In all vertebrates, nodal family members have specific waves of expression required for tissue specification and axis formation. In Xenopus laevis , six nodal genes are expressed before gastrulation, raising the question of whether they have specific roles or act redundantly with each other. Here, we examine the role of Xnr5. We find it acts at the late blastula stage as a mesoderm inducer and repressor of ectodermal gene expression, a role it shares with Vg1. However, unlike Vg1, Xnr5 depletion reduces the expression of the nodal family member xnr1 at the gastrula stage. It is also required for left/right laterality by controlling the expression of the laterality genes xnr1, antivin ( lefty ) and pitx2 at the tailbud stage. In Xnr5-depleted embryos, the heart field is established normally, but symmetrical reduction in Xnr5 levels causes a severely stunted midline heart, first evidenced by a reduction in cardiac troponin mRNA levels, while left-sided reduction leads to randomization of the left/right axis. This work identifies Xnr5 as the earliest step in the signalling pathway establishing normal heart laterality in Xenopus .

Different types of contractions in rat colon and their modulation by oxidative stress

2001 ◽  
Vol 280 (4) ◽  
pp. G546-G554 ◽  
Author(s):  
Asensio Gonzalez ◽  
Sushil K. Sarna
Keyword(s):  
Potential Role ◽  
Contractile Response ◽  
Circular Muscle ◽  
Distal Colon ◽  
Proximal Colon ◽  
Rat Colon ◽  
Hla B27 ◽  
Different Types

The aim of this study was to investigate the modulation of in vitro rat colonic circular muscle contractions by dextran sodium sulfate (DSS)-induced inflammation and in spontaneous inflammation in HLA-B27 rats. We also examined the potential role of hydrogen peroxide (H2O2) in modulating excitation-contraction coupling. The muscle strips from the middle colon generated spontaneous phasic contractions and giant contractions (GCs), the proximal colon strips generated primarily phasic contractions, and the distal colon strips were mostly quiescent. The spontaneous phasic contractions and GCs were not affected by inflammation, but the response to ACh was suppressed in DSS-treated rats and in HLA-B27 rats. H2O2production was increased in the muscularis of the inflamed colon. Incubation of colonic muscle strips with H2O2suppressed the spontaneous phasic contractions and concentration and time dependently reduced the response to ACh; in the middle colon, it also increased the frequency of GCs. We conclude that H2O2mimics the suppression of the contractile response to ACh in inflammation. H2O2also selectively suppresses phasic contractions and increases the frequency of GCs, as found previously in inflamed dog and human colons.

Intestinal distribution of human Na+/H+ exchanger isoforms NHE-1, NHE-2, and NHE-3 mRNA

1996 ◽  
Vol 271 (3) ◽  
pp. G483-G493 ◽  
Author(s):  
P. K. Dudeja ◽  
D. D. Rao ◽  
I. Syed ◽  
V. Joshi ◽  
R. Y. Dahdal ◽  
...  
Keyword(s):  
Small Intestine ◽  
Vertical Axis ◽  
Distal Colon ◽  
Proximal Colon ◽  
Hybridization Technique ◽  
Mrna Levels ◽  
Human Intestine ◽  
Relative Contribution ◽  
Specific Localization ◽  
Ribonuclease Protection

The identity of Na+/H+ exchanger (NHE) isoforms in the human small intestine and colon and their role in vectorial Na+ absorption are not known. The present studies were undertaken to examine the regional and vertical axis distribution of NHE-1, NHE-2, and NHE-3 mRNA in the human intestine. Ribonuclease protection assays were used to quantitate the levels of mRNA of these isoforms in various regions of the human intestine. In situ hybridization technique was used to localize NHE-2 and NHE-3 mRNA in the colon. The NHE-1 isoform message was present uniformly throughout the length of the human intestine. In contrast, mRNA levels for human NHE-2 and NHE-3 isoforms demonstrated significant regional differences. The NHE-3 abundance was found in decreasing order: ileum > jejunum > proximal colon = distal colon. The NHE-2 message level in the distal colon was significantly higher than in the proximal colon but was evenly distributed in the small intestine. In addition, NHE-2 mRNA was present in surface epithelial cells as well as in cells of the crypt region, suggesting the presence of NHE-2 message throughout the vertical axis of the colonic crypts. In contrast, NHE-3 mRNA was localized to surface colonocytes in the proximal colon. On the basis of this tissue-specific localization of NHE-2 and NHE-3 mRNA, it can be speculated that the relative contribution of NHE-2 and NHE-3 isoforms in Na+ absorption in the human intestine may be region specific, and these putative apical isoforms may be differentially regulated.

The Role of Arginine Vasopressin (AVP) in Urinary Free Water Excretion after Saline Drinks

1982 ◽  
Vol 63 (3) ◽  
pp. 47P-48P
Author(s):  
J. Brown ◽  
H.P. Henneberry ◽  
J.D.H. Slater
Keyword(s):  
Arginine Vasopressin ◽  
Free Water ◽  
Water Excretion

scholarly journals Mouse Models and the Urinary Concentrating Mechanism in the New Millennium

2007 ◽  
Vol 87 (4) ◽  
pp. 1083-1112 ◽  
Author(s):  
Robert A. Fenton ◽  
Mark A. Knepper
Keyword(s):  
Water Conservation ◽  
Collecting Duct ◽  
Tubuloglomerular Feedback ◽  
Water Excretion ◽  
Renal Transporters ◽  
Concentrating Mechanism ◽  
New Information ◽  
Renal Micropuncture ◽  
Key Questions

Our understanding of urinary concentrating and diluting mechanisms at the end of the 20th century was based largely on data from renal micropuncture studies, isolated perfused tubule studies, tissue analysis studies and anatomical studies, combined with mathematical modeling. Despite extensive data, several key questions remained to be answered. With the advent of the 21st century, a new approach, transgenic and knockout mouse technology, is providing critical new information about urinary concentrating processes. The central goal of this review is to summarize findings in transgenic and knockout mice pertinent to our understanding of the urinary concentrating mechanism, focusing chiefly on mice in which expression of specific renal transporters or receptors has been deleted. These include the major renal water channels (aquaporins), urea transporters, ion transporters and channels (NHE3, NKCC2, NCC, ENaC, ROMK, ClC-K1), G protein-coupled receptors (type 2 vasopressin receptor, prostaglandin receptors, endothelin receptors, angiotensin II receptors), and signaling molecules. These studies shed new light on several key questions concerning the urinary concentrating mechanism including: 1) elucidation of the role of water absorption from the descending limb of Henle in countercurrent multiplication, 2) an evaluation of the feasibility of the passive model of Kokko-Rector and Stephenson, 3) explication of the role of inner medullary collecting duct urea transport in water conservation, 4) an evaluation of the role of tubuloglomerular feedback in maintenance of appropriate distal delivery rates for effective regulation of urinary water excretion, and 5) elucidation of the importance of water reabsorption in the connecting tubule versus the collecting duct for maintenance of water balance.

scholarly journals Prophylactic hemoclips in prevention of delayed post-polypectomy bleeding for ≥ 1 cm colorectal polyps: meta-analysis of randomized controlled trials

2020 ◽  
Vol 08 (09) ◽  
pp. E1102-E1110
Author(s):  
Faisal Kamal ◽  
Muhammad A. Khan ◽  
Salman Khan ◽  
Hemnishil K. Marella ◽  
Tamara Nelson ◽  
...  
Keyword(s):  
Randomized Controlled Trials ◽  
Lower Risk ◽  
Meta Analysis ◽  
Distal Colon ◽  
Proximal Colon ◽  
Controlled Trials ◽  
Colon Polyps ◽  
Randomized Controlled ◽  
Significant Difference

Abstract Background and aim Studies evaluating the role of prophylactic hemoclips (HC) in prevention of delayed post-polypectomy bleeding (DPPB) have reported conflicting results. We conducted a meta-analysis of randomized controlled trials (RCTs) to evaluate the role of prophylactic HC placement in prevention of DPPB for polyps ≥ 1 cm in size. Methods We reviewed several databases to identify RCTs evaluating the role of HC in prevention of DPPB. The outcomes assessed included prevention of DPPB with polyps 1 to 1.9 cm, ≥ 2 cm, any polyp ≥ 1 cm, proximal colon polyps, distal colon polyps, and perforation. We analyzed data using a fixed effect model and reported summary pooled risk ratios (RR) with 95 % confidence intervals (CI). We assessed heterogeneity with the I2 statistic. Results We included nine RCTs with 4550 patients. For polyps ≥ 2 cm, there was a statistically significantly lower risk of DPPB with use of HC; RR 0.55, 95 % CI 0.36, 0.86. There was also a statistically significantly lower risk for proximal colon polyps ≥ 2 cm; RR 0.41 (0.24, 0.70) but no significant difference for distal polyps; RR 1.23 (0.45, 3.32). There was also no significant difference in risk for polyps 1 to 1.9 cm; RR 1.07 (0.59, 1.97). There was no significant reduction in risk of perforation with HC use for any polyp size. Conclusions Prophylactic HC placement is effective in prevention of DPPB from proximal colon polyps ≥ 2 cm, but of no significant benefit for polyps 1 to 1.9 cm in size or for distal colon polyps ≥ 2 cm.

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