scholarly journals Glucocorticoids increase salt appetite by promoting water and sodium excretion

2007 ◽  
Vol 293 (3) ◽  
pp. R1444-R1451 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Saline Solution ◽  
Salt Appetite ◽  
Total Fluid Intake ◽  
Glucocorticoid Treatment ◽  
Water Excretion ◽  
Sodium Ingestion ◽  
Water And Sodium Excretion ◽  
The Brain

Glucocorticoids [e.g., corticosterone and dexamethasone (Dex)], when administered systemically, greatly increase water drinking elicited by angiotensin and sodium ingestion in response to mineralocorticoids [e.g., aldosterone and deoxycorticosterone acetate (DOCA)], possibly by acting in the brain. In addition, glucocorticoids exert powerful renal actions that could influence water and sodium ingestion by promoting their excretion. To test this, we determined water and sodium intakes, excretions, and balances during injections of Dex and DOCA and their coadministration (DOCA+Dex) at doses commonly employed to stimulate ingestion of water and sodium. In animals having only water to drink, Dex treatment greatly increased water and sodium excretion without affecting water intake, thereby producing negative water and sodium balances. Similar results were observed when Dex was administered together with DOCA. In animals having water and saline solution (0.3 M NaCl) to drink, Dex treatment increased water and sodium excretion, had minimal effects on water and sodium intakes, and was associated with negative water and sodium balances. DOCA treatment progressively increased sodium ingestion, and both water and sodium intakes exceeded their urinary excretion, resulting in positive water and sodium balances. The combination of DOCA+Dex stimulated rapid, large increases in sodium ingestion and positive sodium balances. However, water excretion outpaced total fluid intake, resulting in large, negative water balances. Plasma volume increased during DOCA treatment and did not change during treatment with Dex or DOCA+Dex. We conclude that increased urinary excretion, especially of water, during glucocorticoid treatment may explain the increased ingestion of water and sodium that occurs during coadministration with mineralocorticoids.

Biphasic effects of ANP infusion in conscious, euvolumic rats: roles of AQP2 and ENaC trafficking

2006 ◽  
Vol 290 (2) ◽  
pp. F530-F541 ◽  
Author(s):  
Weidong Wang ◽  
Chunling Li ◽  
Lene N. Nejsum ◽  
Hongyan Li ◽  
Soo Wan Kim ◽  
...  
Keyword(s):  
Subcellular Localization ◽  
Sodium Excretion ◽  
Na Channel ◽  
Volume Depletion ◽  
Water Excretion ◽  
Body Sodium ◽  
Urine Production ◽  
Collecting Ducts ◽  
Water And Sodium Excretion ◽  
Epithelial Na Channel

Atrial natriuretic peptide (ANP) acutely promotes water and sodium excretion, whereas subchronic effects involve water retention. Renal hemodynamics, water and sodium excretion, and aquaporin-2 (AQP2) and epithelial Na channel (ENaC) subcellular trafficking were determined in response to continuous ANP infusion in conscious rats, where body sodium and fluid balance was constantly maintained. ANP (0.5 μg·kg−1·min−1) evoked a transient (peak at 10 min) fivefold diuresis followed by reduced urine production to control levels (30- to 90-min period). The fractional distal water excretion was significantly increased initially and then decreased in response to ANP. There was no change in the subcellular localization of AQP2 and AQP2 phosphorylated in PKA consensus site S256 (p-AQP2) 10 min after ANP infusion. In contrast, after 90 min a marked increase in apical labeling of AQP2 and p-AQP2 was observed in the inner and outer medullary collecting ducts but not in cortical collecting ducts. In support of this, ANP induced plasma membrane targeting of AQP2 in transiently AQP2-transfected cells. ANP infusion evoked an instant increase in renal sodium excretion, which persisted for 90 min. Ten minutes of ANP infusion induced no changes in the subcellular localization of ENaC subunits, whereas a marked increase in apical targeting of α- and γ-subunits was observed after 90 min. In conclusion, 1) ANP infusion induced a sustained natriuresis and transient diuresis; 2) there were no changes in the subcellular localization of AQP2 and ENaC subunits after 10 min of ANP infusion; and 3) there was a marked increase in apical targeting of AQP2, p-AQP2, and α- and γ-ENaC after 90 min of ANP infusion. The increased targeting of ENaC and AQP2 likely represents direct or compensatory effects to increase sodium and water reabsorption and to prevent volume depletion in response to prolonged ANP infusion.

Abrupt changes of water and sodium excretion in normal and adrenalectomized dogs

1960 ◽  
Vol 199 (2) ◽  
pp. 275-280 ◽  
Author(s):  
R. D. Berlin ◽  
A. C. Barger ◽  
F. P. Muldowney ◽  
G. O. Barnett
Keyword(s):  
Hormone Therapy ◽  
Sodium Excretion ◽  
Water Diuresis ◽  
Water Excretion ◽  
Excretion Pattern ◽  
Identical Response ◽  
Abrupt Changes ◽  
Rapid Changes ◽  
Adrenal Cortical Hormone ◽  
Water And Sodium Excretion

An experiment was designed to induce rapid changes in sodium and water excretion. With this procedure normal dogs showed a prompt and marked water diuresis, with an accompanying antinatriuresis. The same dogs, adrenalectomized and maintained on constant adrenal cortical hormone therapy, demonstrated an identical response despite the constancy of steroid concentration, suggesting a ‘permissive’ action of the hormones. When the animals were deprived of therapy for several days the excretion patterns of sodium and water did become markedly abnormal. Acute replacement with hydrocortisone restored the water excretion pattern to normal but did not correct the abnormal sodium excretion pattern. Aldosterone, given prior to and during the experiment, failed to restore either the water or sodium excretion patterns. The results obtained with acute replacement of hydrocortisone and aldosterone were identical with those obtained with hydrocortisone alone.

Fos expression in rat brain during depletion-induced thirst and salt appetite

1998 ◽  
Vol 274 (6) ◽  
pp. R1807-R1814 ◽  
Author(s):  
R. L. Thunhorst ◽  
Z. Xu ◽  
M. Z. Cicha ◽  
A. M. Zardetto-Smith ◽  
A. K. Johnson
Keyword(s):  
Low Dose ◽  
Physiological State ◽  
Subcutaneous Administration ◽  
Neural Activation ◽  
Lamina Terminalis ◽  
Salt Appetite ◽  
Fos Protein ◽  
Sodium Ingestion ◽  
Dependent Model ◽  
The Brain

The expression of Fos protein (Fos immunoreactivity, Fos-ir) was mapped in the brain of rats subjected to an angiotensin-dependent model of thirst and salt appetite. The physiological state associated with water and sodium ingestion was produced by the concurrent subcutaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Furo/Cap treatment). The animals were killed 2 h posttreatment, and the brains were processed for Fos-ir to assess neural activation. Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation. Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately. Fos-ir was reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain. The present work provides further evidence that areas of lamina terminalis subserve angiotensin-dependent thirst and salt appetite.

Alpha 2-adrenoceptor antagonism of vasopressin-induced changes in sodium excretion

1985 ◽  
Vol 248 (6) ◽  
pp. F767-F772 ◽  
Author(s):  
D. D. Smyth ◽  
S. Umemura ◽  
W. A. Pettinger
Keyword(s):  
Adenylate Cyclase ◽  
Sodium Excretion ◽  
Rat Kidney ◽  
Water Excretion ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Regulatory Systems ◽  
Adrenoceptor Agonists ◽  
Induced Changes ◽  
Water And Sodium Excretion

Alpha 2-adrenoceptor agonists attenuate vasopressin-mediated changes in water excretion. The effects on sodium excretion, however, are unclear. We therefore utilized the nonrecirculating isolated perfused rat kidney to study the direct effects of vasopressin and alpha 2-adrenoceptor stimulation on sodium and water excretion in the absence of systemic regulatory systems. The perfusate was a Krebs-Henseleit solution (3.5 g/100 ml Ficoll; 1.0% albumin; 36 degrees C) containing prazosin (30 nM) and propranolol (100 nM) to prevent effects of alpha 1- and beta-adrenoceptor stimulation. Vasopressin (10 microU/ml) produced a significant (P less than 0.05) decrease in both water and sodium excretion. Potassium excretion was not significantly altered. Alpha 2-Adrenoceptor stimulation with l-epinephrine (28 nM) reversed (P less than 0.05) the effects of vasopressin on water and sodium excretion. To confirm that this attenuation was mediated by alpha 2-adrenoceptors, an alpha 2-adrenoceptor antagonist, yohimbine, was administered. Yohimbine (300 nM) blocked the effects of epinephrine on sodium and water excretion (P less than 0.05). The adenosine P-site agonist, SQ 22,536 (100 microM), which mediates its effects through inhibition of adenylate cyclase, produced the same reversal as that of epinephrine on vasopressin-mediated changes. Thus alpha 2-adrenoceptor stimulation antagonized the effects of vasopressin on both water and sodium excretion at the renal level. A corollary to this conclusion is that the function-specific activation of renal adenylate cyclase determines the effect of alpha 2-adrenoceptor stimulation.

Effects of subfornical organ lesions on acutely induced thirst and salt appetite

1999 ◽  
Vol 277 (1) ◽  
pp. R56-R65 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Enzyme Inhibitor ◽  
Extracellular Fluid ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Ang Ii ◽  
Electrolytic Lesions ◽  
Sodium Ingestion ◽  
Second Procedure ◽  
The Brain

We examined the role of the subfornical organ (SFO) in stimulating thirst and salt appetite using two procedures that initiate water and sodium ingestion within 1–2 h of extracellular fluid depletion. The first procedure used injections of a diuretic (furosemide, 10 mg/kg sc) and a vasodilator (minoxidil, 1–3 mg/kg ia) to produce hypotension concurrently with hypovolemia. The resulting water and sodium intakes were inhibited by intravenous administration of ANG II receptor antagonist (sarthran, 8 μg ⋅ kg−1 ⋅ min−1) or angiotensin-converting enzyme inhibitor (captopril, 2.5 mg/h). The second procedure used injections of furosemide (10 mg/kg sc) and a low dose of captopril (5 mg/kg sc) to initiate water and sodium ingestion upon formation of ANG II in the brain. Electrolytic lesions of the SFO greatly reduced the water intakes, and nearly abolished the sodium intakes, produced by these relatively acute treatments. These results contrast with earlier findings showing little effect of SFO lesions on sodium ingestion after longer-term extracellular fluid depletion.

scholarly journals Inhibition of heme oxygenase augments tubular sodium reabsorption

2011 ◽  
Vol 300 (4) ◽  
pp. F941-F946 ◽  
Author(s):  
Keith E. Jackson ◽  
Debra W. Jackson ◽  
Syed Quadri ◽  
Marshall J. Reitzell ◽  
L. Gabriel Navar
Keyword(s):  
Arterial Pressure ◽  
Heme Oxygenase ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Plasma Renin ◽  
Sodium Reabsorption ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Oxide Synthase ◽  
Water And Sodium Excretion

Heme oxygenase (HO) catalyzes the degradation of heme to form iron, biliverdin, and carbon monoxide (CO). The vascular actions of CO include direct vasodilation of vascular smooth muscle and indirect vasoconstriction through inhibition of nitric oxide synthase (NOS). This study was performed to examine the effects in the kidney of inhibition of heme oxygenase alone or combined with NOS inhibition. Chromium mesoporphyrin (CrMP; 45 μmol/kg ip), a photostable HO inhibitor, was given to control rats and NG-nitro-l-arginine methyl ester (l-NAME)-treated hypertensive rats (50 mg·kg−1·day−1, 12 h, 4 days). In control animals, CrMP decreased CO levels, renal HO-1 levels, urine volume, and sodium excretion, but had no effect on arterial pressure, renal blood flow (RBF), plasma renin activity (PRA), or glomerular filtration rate (GFR). In l-NAME-treated hypertensive rats, CrMP decreased endogenous CO and renal HO-1 levels and had no effect on arterial pressure, RBF, or GFR but decreased sodium and water excretion in a similar manner to control animals. An increase in PRA was observed in untreated rats but not in l-NAME-infused rats, indicating that this effect is associated with an absent NO system. The results suggest that inhibition of HO promotes water and sodium excretion by a direct tubular action that is independent of renal hemodynamics or the NO system.

Renal nerves and postprandial renal excretion in the conscious monkey

1991 ◽  
Vol 261 (5) ◽  
pp. R1197-R1203 ◽  
Author(s):  
T. V. Peterson ◽  
B. A. Benjamin ◽  
N. L. Hurst ◽  
C. G. Euler
Keyword(s):  
Urinary Excretion ◽  
Nonhuman Primate ◽  
Nasogastric Tube ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Renal Excretion ◽  
Renal Nerves ◽  
Electrolyte Excretion ◽  
Macaque Monkeys ◽  
High Sodium

Experiments were performed in conscious macaque monkeys to determine if the renal nerves are important in mediating postprandial increases in renal fluid-electrolyte excretion in this species. Monkeys were given a high-sodium meal via a nasogastric tube. Consecutive 10-min urine samples were taken during the 30-min time of meal administration and then 180 min postprandially. The experiment was performed both before and 10-14 days after each animal underwent renal denervation. Diuresis and natriuresis occurred under both renal-innervated and -denervated conditions. However, the amounts of urine and sodium excreted were less after renal denervation. For the total 210 min of measurements obtained after the meal was started, cumulative urine output was 95.0 +/- 26.4 ml and sodium excretion 7.18 +/- 1.74 meq in innervated kidneys vs. 56.7 +/- 7.0 ml (a 40% decrease; P less than 0.005) and 4.84 +/- 0.99 meq (a 33% decrease; P less than 0.01) after denervation. These results demonstrate that the renal nerves are important in the nonhuman primate for eliciting the postprandial changes in urinary excretion secondary to intake of a high-sodium meal.

Acute renal denervation produces a diuresis and natriuresis in young SHR but not WKY rats

1986 ◽  
Vol 251 (4) ◽  
pp. F655-F661 ◽  
Author(s):  
M. A. Rudd ◽  
R. S. Grippo ◽  
W. J. Arendshorst
Keyword(s):  
Sodium Excretion ◽  
Renal Denervation ◽  
Strain Differences ◽  
Urine Flow ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Water Excretion ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Clearance experiments were conducted to determine the effect of acute unilateral renal denervation (DNX) on renal hemodynamics and salt and water excretion in anesthetized 6-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto genetic control rats (WKY). Before DNX, SHR had higher mean arterial pressure (33%) and renal vascular resistance (RVR) (57%) and lower glomerular filtration rate (GFR) (10%); urine flow and sodium excretion were similar. Following DNX in SHR, sodium and water excretion increased by 138 and 62%, respectively (P less than 0.001); GFR and RVR were unchanged. In contrast, DNX in WKY did not affect urine flow (0%) or sodium excretion (-21%). These strain differences were observed in Okamoto-Aoki rats from two sources. Effective DNX was indicated by 95% reduction of norepinephrine content 3 days after DNX in both strains. Six-week-old Sprague-Dawley and Munich-Wistar rats, in contrast to WKY, responded to DNX with a natriuresis (+182%) and diuresis (+95%) (P less than 0.001). Renal function was unaffected by sham DNX in SHR. Our results indicate that efferent renal nerve activity has little tonic influence on the renal vasculature in these young rats. Augmented neurotransmitter release and/or tubular responsiveness may be involved in fluid and electrolyte retention and the pathogenesis of hypertension in SHR. Conversely, blunted renal neuroeffector responses may prevent WKY from developing hypertension.

the Comparred Effect of Zyprasidone and Haloperidol at Hippocampal and Frontal Cortex at Rats

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
D. Marinescu ◽  
L. Mogoanta ◽  
T. Udristoiu
Keyword(s):  
Adverse Event ◽  
Frontal Cortex ◽  
Negative Symptoms ◽  
Structural Changes ◽  
Saline Solution ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
D2 Receptors ◽  
Cerebral Structure ◽  
The Brain

Background:The alteration of hippocampal and prefrontal structures is linked with schizophrenia cognitive impairment and negative symptoms. the antipsychotics can induced apoptotic mechanisms correlated with the psychopharmacological mechanism of excesive blocking of the D2 receptors. Distress determined increase of the glucocorticoid aggression wich drive to the decrease of neuroprotective capacity at the brain level.Methods:We formed 5 study lots (5 adults rats) and a control lot. the substancies were administrated intraperitoneal, daily, saline solution equivalent to: ziprasidone (1.25mg/kg/day) and haloperidole (0.20mg/kg/day), dexametasone (0.20mg/kg/day):N1 - Haloperidole; N2 - Dexametasone; N3 - Ziprasidone; N4 - Dexametasone and Haloperidole; N5 - Dexametasone and Ziprasidone; N6 -control lot.We monitorised the cardiovascular function, respiration and EPS, without signaling any serious deadly adverse event. the rats were sacrificed during the 10th day and 21th day.Results:Frontal cortex and hippocamp were the most intensely affected even since the 10-th day to the N4 (haloperidole and dexametasone) lot with massive neuronal loss at the VI, V, and IV frontal cerebral layers.The lots treated with ziprasidone presented significant lesser structural changes in frontal cortex and hippocamp, comparative to haloperidole. the lots treated with dexametasone and ziprasidone (N5) are lesser affected at the cerebral structure level.Conclusions:Haloperidole has a significant decrease in neuroprotection. Ziprasidone demonstrated an neuroprotective effect.

Sign in / Sign up

Export Citation Format

Share Document