scholarly journals Upregulation of Intestinal NHE3 Following Saline Ingestion

2013 ◽  
Vol 37 (1) ◽  
pp. 48-57 ◽  
Author(s):  
Venkanna Pasham ◽  
Anand Rotte ◽  
Shuchen Gu ◽  
Wenting Yang ◽  
Madhuri Bhandaru ◽  
...  
Keyword(s):  
Saline Ingestion

Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats

1995 ◽  
Vol 269 (2) ◽  
pp. R245-R251 ◽  
Author(s):  
R. E. Blackburn ◽  
W. K. Samson ◽  
R. J. Fulton ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Osmolality ◽  
Plasma Sodium ◽  
Salt Appetite ◽  
Saline Ingestion ◽  
A Chain ◽  
Anp Receptors ◽  
Atrial Natriuretic

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.

Cardiovascular and sweating responses to water ingestion during dehydration

1965 ◽  
Vol 20 (5) ◽  
pp. 975-979 ◽  
Author(s):  
Leo C. Senay ◽  
Margaret L. Christensen
Keyword(s):  
Blood Flow ◽  
The Body ◽  
Evaporative Heat Loss ◽  
Cutaneous Blood Flow ◽  
Temperature Changes ◽  
Fluid Ingestion ◽  
Water Ingestion ◽  
Heat Chamber ◽  
Saline Ingestion ◽  
Cutaneous Blood

The experiments reported are concerned with cardiovascular and sudomotor events preceding, accompanying, and following ingestion of water by five dehydrating subjects 8.75 hr after entrance into a heat chamber (43.3 C DB, 29 C WB). Certain skin areas such as the cheek showed increases in evaporative heat loss before subjects came in contact with water. This reflex could be initiated by saline ingestion but the degree of skin and oral temperature changes appeared to depend on tonicity of fluid ingested. The gustatory reflex was not thought to be the initiating agent for sudomotor responses. Increases in cutaneous blood flow appeared to begin almost as promptly as sweating responses but took considerably longer to develop. Ingestion of saline, though initiating a sweating response, did not alter heart rate, blood pressure, or cutaneous blood flow. It is suggested that fluid ingestion, regardless of tonicity, triggers reflex sweating over the body surface. Intensity and duration of this sudomotor response, as well as initiation of cardiovascular changes, apparently depend on tonicity of ingested fluid. cutaneous blood flow; skin temperature; regional sweating Submitted on November 27, 1964

Some parameters of sucrose and saline ingestion

1970 ◽  
Vol 5 (6) ◽  
pp. 663-666 ◽  
Author(s):  
Khalil A. Khavari
Keyword(s):  
Saline Ingestion

Desalivation and saline ingestion in rats

1977 ◽  
Vol 19 (1) ◽  
pp. 130-134 ◽  
Author(s):  
Roderick Wong ◽  
Leon Kraintz
Keyword(s):  
Saline Ingestion

Hypothalamic lesions increase saline ingestion induced by injection of angiotensin II into AV3V in rats

1991 ◽  
Vol 261 (3) ◽  
pp. R647-R651 ◽  
Author(s):  
L. A. Camargo ◽  
W. A. Saad ◽  
A. Renzi ◽  
L. A. de Luca Junior ◽  
J. R. Goncalves ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Third Ventricle ◽  
Ventromedial Nucleus ◽  
Electrolytic Lesion ◽  
Partial Recovery ◽  
Ang Ii ◽  
Receptor Antagonists ◽  
Hypothalamic Lesions ◽  
Saline Ingestion

Water and 3% NaCl intake were increased by the injection of 4 ng angiotensin II (ANG II) into the anteroventral third ventricle (AV3V) region of rats. Pretreatment with two specific ANG II receptor antagonists, [octanoyl-Leu8]ANG II and [Leu8]ANG II, significantly reduced ANG II-induced water and saline intake. This inhibition lasted approximately 30 min, with partial recovery at 60 min. In rats with electrolytic lesion of the bilateral ventromedial nucleus of hypothalamus (VMH), the effect of ANG II on water intake was not different from that observed in sham rats, but saline ingestion increased. In summary, the present results show that the AV3V region is an important central structure for ANG II-induced saline ingestion. Lesion of the VMH increases the response to ANG II, showing an interaction between the AV3V region and the VMH in the regulation of salt ingestion.

scholarly journals Pilot study: Trehalose-induced remodelling of the human microbiota affects Clostridioides difficile infection outcome in an in vitro colonic model

2021 ◽  
Author(s):  
Anthony M. Buckley ◽  
Ines B. Moura ◽  
Norie Arai ◽  
William Spittal ◽  
Emma Clark ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Intestinal Tract ◽  
Enhanced Recovery ◽  
Human Gut ◽  
Human Microbiota ◽  
Clostridioides Difficile ◽  
Clostridioides Difficile Infection ◽  
Saline Ingestion ◽  
Human Intestinal Tract

AbstractWithin the human intestinal tract, dietary, microbial- and host-derived compounds are used as signals by many pathogenic organisms, including Clostridioides difficile. Trehalose has been reported to enhance virulence of certain C. difficile ribotypes; however, such variants are widespread and not correlated with clinical outcomes for patients suffering from C. difficile infection (CDI). Here, we make preliminary observations to how to trehalose supplementation affects the microbiota in an in vitro model and show that trehalose can reduce the outgrowth of C. difficile, preventing simulated CDI. Three clinically reflective human gut models simulated the effects of sugar (trehalose or glucose) or saline ingestion on the microbiota. Models were instilled with sugar or saline and further exposed to C. difficile spores. The recovery of the microbiota following antibiotic treatment and CDI induction was monitored in each model. The human microbiota remodeled to utilise the bioavailable trehalose. Clindamycin induction caused simulated CDI in models supplemented with either glucose or saline; however, trehalose supplementation did not result in CDI, although limited spore germination did occur. The absence of CDI in trehalose model was associated with enhanced abundances of Finegoldia, Faecalibacterium and Oscillospira, and reduced abundances of Klebsiella and Clostridium spp., compared with the other models. Functional analysis of the microbiota in the trehalose model revealed differences in the metabolic pathways, such as amino acid metabolism, which could be attributed to prevention of CDI. Our data show that trehalose supplementation remodelled the microbiota, which prevented simulated CDI, potentially due to enhanced recovery of nutritionally competitive microbiota against C. difficile.

Hypothalamic lesions abolish cardiovascular responses to chronic saline ingestion

1983 ◽  
Vol 244 (6) ◽  
pp. R751-R757
Author(s):  
S. Sasaki ◽  
R. D. Bunag
Keyword(s):  
Saline Solution ◽  
Isotonic Saline ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Ventromedial Hypothalamus ◽  
Neural Firing ◽  
Salt Loading ◽  
Pressor Responses ◽  
Saline Ingestion ◽  
Bilateral Destruction

In rats made to drink isotonic saline solution instead of water for 5 wk, systolic pressure and heart rate, whether recorded indirectly from the tail or directly from femoral catheters, rose slightly. When the ventromedial hypothalamus was stimulated electrically, increases in arterial pressure and sympathetic neural firing were larger in saline-drinking than in water-drinking rats. By contrast, pressor responses to injections of norepinephrine or tyramine were unaltered. Following bilateral destruction of the ventromedial hypothalamus in other rats, none of the effects of chronic saline ingestion was elicited. Although neither the site nor the mechanism causing sympathetic overactivity has been determined, our results are in accord with the interpretation that salt loading elevates blood pressure, at least in part, by stimulating the ventromedial hypothalamus to increase sympathetic activity.

Transcapillary fluid responses to lower body negative pressure

1993 ◽  
Vol 74 (6) ◽  
pp. 2763-2770 ◽  
Author(s):  
M. Aratow ◽  
S. M. Fortney ◽  
D. E. Watenpaugh ◽  
A. G. Crenshaw ◽  
A. R. Hargens
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Whole Body ◽  
Chamber Pressure ◽  
Fluid Loss ◽  
Lower Body ◽  
Urine Production ◽  
Saline Ingestion

The effect of lower body negative pressure (LBNP) on transcapillary fluid balance is unknown. Therefore, our objective was to assess leg interstitial fluid pressures (IFP), leg circumference, plasma volume (PV), and net whole body transcapillary fluid transport (TFT) during and after supine LBNP and to evaluate the addition of oral saline ingestion on transcapillary exchange. Six healthy men 23–41 yr old underwent 4 h of 30 mmHg LBNP, followed by 50 min of supine recovery on two separate occasions, once with and once without ingestion of 1 liter of isotonic saline. IFP was measured continuously in subcutis as well as superficial and deep regions of the tibialis anterior muscle by slit catheters. TFT was calculated by subtracting urine production and calculated insensible fluid loss from changes in PV. During exposure to LBNP, IFP decreased in parallel with chamber pressure, foot venous pressure did not change, leg circumference increased by 3 +/- 0.35% (SE) (P < 0.05), and PV decreased by 14 +/- 2.3%. IFP returned to near control levels after LBNP. At the end of minute 50 of recovery, PV remained decreased (by 7.5 +/- 5.2%) and leg circumference remained elevated (by 1 +/- 0.37%). LBNP alone produced significant movement of fluid into the lower body but no net TFT (-7 +/- 12 ml/h). During LBNP with saline ingestion, 72 +/- 4% of the ingested fluid volume filtered out of the vascular space (TFT = 145 +/- 10 ml/h), and PV decreased by 6 +/- 3%.(ABSTRACT TRUNCATED AT 250 WORDS)

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