scholarly journals Effect of volume expansion with hypertonic- and isotonic saline and isotonic glucose on sodium and water transport in the principal cells in the kidney

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
Janni M Jensen ◽  
Frank H Mose ◽  
Jesper N Bech ◽  
Soren Nielsen ◽  
Erling B Pedersen
Keyword(s):  
Water Transport ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Principal Cells

Roles of cephalic Na+ concentration and urodilatin in control of renal Na+ excretion

1992 ◽  
Vol 262 (3) ◽  
pp. F513-F516 ◽  
Author(s):  
C. Emmeluth ◽  
C. Drummer ◽  
R. Gerzer ◽  
P. Bie
Keyword(s):  
Renal Function ◽  
Volume Expansion ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Isotonic Saline ◽  
Fold Increase ◽  
Sodium Concentration ◽  
Fourfold Increase ◽  
Infusion Technique ◽  
Water Contents

Effects on renal function of an increase in the concentration of sodium in the blood supplying the head were investigated in water-diuretic conscious dogs in which the sodium and water contents were controlled by separate servo-mechanisms. A selective 2% increase in the sodium concentration of the carotid blood was achieved by a split-infusion technique including infusions of hypertonic saline into both carotid arteries and water into a jugular vein at rates making the combined infusate isotonic. This procedure caused a 34-fold increase in renal sodium excretion concomitant with a fourfold increase in the rate of urinary excretion of urodilatin. A comparable isotonic volume expansion (isotonic saline infusion into carotid arteries and jugular vein) caused a significantly smaller (13-fold) increase in urinary rate of excretion of sodium (P less than 0.02) and no increase at all in the excretion of urodilatin. It is hypothesized that cephalic sodium concentration receptors regulate the rate of excretion of sodium via urodilatin even under the present slightly hypotonic conditions.

scholarly journals Phosphodiesterase inhibitors correct resistance to natriuretic peptides in rats with Heymann Nephritis.

1996 ◽  
Vol 7 (4) ◽  
pp. 582-593
Author(s):  
J P Valentin ◽  
W Z Ying ◽  
L A Sechi ◽  
K T Ling ◽  
C Qiu ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Phosphodiesterase Inhibitors ◽  
Contralateral Kidney ◽  
Heymann Nephritis

Experimental nephrotic syndrome is characterized by abnormal sodium metabolism, reflected in a blunted natriuretic response both to volume expansion and to infused atrial natriuretic peptide (ANP). The studies presented here examined the relationships among plasma ANP concentration and urinary sodium (VNaV) and cyclic GMP excretion (UcGMPV) in vivo, and the responsiveness of isolated glomeruil and inner medullary collecting duct (IMCD) cells to ANP and urodilatin (renal natriuretic peptide; RNP) in vitro in rats with Heymann nephritis, an immunologically mediated model of nephrotic syndrome. Nine to 14 days after Ip injection of anti-Fx1A antiserum, rats were proteinuric and had a blunted natriuretic response to intravenous infusion of isotonic saline (2% body weight, given over 5 min). Thirty min after the onset of the infusion, plasma ANP concentration was increased to the same extent in both normal and nephritic rats, compared with their respective hydropenic controls. Despite this increase, UcGMPV was significantly less in nephritic rats after the saline infusion. Accumulation of cGMP by isolated glomeruil and IMCD cells from nephritic rats after incubation with ANP and RNP was also significantly reduced, compared with normal rats. This difference was not related to differences in either density or affinity of renal ANP receptors, but was abolished when accumulation of cGMP was measured in the presence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhibitors of cyclic nucleotide phosphodiesterases (PDE). Infusion of Zaprinast into one renal artery in nephritic rats normalized both the natriuretic response to volume expansion and the increase in UcGMPV from the infused, but not the contralateral, kidney. Furthermore, cGMP-PDE activity was increased in IMCD cell homogenates from nephritic compared with normal rats (388 +/- 32 versus 198 +/- 93 pmol/min per mg protein, P < 0.03). These results indicate that blunted volume expansion natriuresis accompanied by cellular resistance to ANP in vitro occurs in an immunologic model of renal injury. The resistance is not related to an alteration in ANP release or binding to its renal receptors, but is suppressed by PDE inhibitors and is associated with increased renal cGMP. PDE activity, thus suggesting that enhanced cGMP-PDE activity may account for resistance to the natriuretic actions of ANP observed in vivo. This defect may represent the intrinsic sodium transport abnormality linked to sodium retention in nephrotic syndrome.

Suppressive action of prolactin on renal response to volume expansion

1975 ◽  
Vol 229 (1) ◽  
pp. 81-85 ◽  
Author(s):  
MS Lucci ◽  
HH Bengele ◽  
S Solomon
Keyword(s):  
Volume Expansion ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Physical Factors ◽  
Water Load ◽  
Renal Response ◽  
Water Handling ◽  
Male Wistar Rats ◽  
Diuretic Response ◽  
Ovine Prolactin

The effects of prolactin on rat renal sodium and water handling during volume expansion were studied using clearance techniques. Both control and experimental adult male Wistar rats were prehydrated with an oral water load of volume equal to 2.5% body weight (BW). At least 3 h later, a continuous intravenous infusion of ovine prolactin (NIH-P-S8), 7.1 mug/h per 100 g, was started in the experimental group. After a 1-h steady-state period, the rats were given an intravenous expansion infusion of either hypotonic saline (2.5% BW), isotonic saline (2.5% and 7.5% BW), or blood (2.5% BW). In all control hypotonic and isotonic saline-expanded animals, within 1 h the rats excreted a volume of urine equal to over 50% of the volume of saline infused. The diuretic and natriuretic responses to saline expansion of prolactin-treated rats were significantly smaller than controls. In contrast to the effects of prolactin on the renal response to saline infusions, it did not alter the natriuretic or diuretic response to blood infusion. Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule.

Systemic inhibition of nitric oxide and prostaglandins in volume-induced natriuresis and hypertension

1998 ◽  
Vol 274 (1) ◽  
pp. R175-R180 ◽  
Author(s):  
James D. Krier ◽  
Juan Carlos Romero
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Significant Elevation ◽  
Synthesis Inhibition ◽  
Anesthetized Dogs ◽  
Change Map

Nitric oxide (NO) synthesis inhibition with N G-nitro-l-arginine methyl ester (l-NAME) (10 μg ⋅ kg−1 ⋅ min−1iv), cyclooxygenase inhibition with meclofenamate (Meclo; 5 mg/kg iv bolus), and combination of drugs (l-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5% body wt over 60 min) in anesthetized dogs. Before VE,l-NAME ( n = 6), Meclo ( n = 6), andl-NAME+Meclo ( n = 6) produced significant increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in Meclo-treated dogs, but produced a significant elevation in the control dogs (14 ± 6 mmHg), inl-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated withl-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 μmol/min),l-NAME (31 ± 9 to 664 ± 65 μmol/min), and Meclo groups (41 ± 10 to 699 ± 51 μmol/min). However, this natriuretic response was attenuated in dogs pretreated with l-NAME+Meclo (12 ± 4 to 185 ± 52 μmol/min). These results indicate that 1) blockade of both NO and PGs has significant diminishing effects on volume-induced natriuresis, 2) NO blockade alone impairs volume-induced natriuresis in a manner that requires further increases in MAP to restore the natriuresis, and 3) PG blockade alone does not curtail volume-induced natriuresis.

Determinants of atrial natriuretic factor secretion in dogs expanded with isotonic saline or colloid solutions

1991 ◽  
Vol 69 (2) ◽  
pp. 145-153
Author(s):  
Peter Cernacek ◽  
Mortimer Levy
Keyword(s):  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Blood Volume ◽  
Bovine Serum ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Though increments in blood volume and atrial pressure are thought to be the primary stimuli for ANF secretion, plasma levels of this peptide do not always behave as a simple function of volume status. To outline the relationship between the latter and cardiac ANF release, we used five different volume-expansion protocols in anesthetized dogs. A stepwise expansion of plasma volume (PV) was achieved by two consecutive infusions: 0.9% saline followed or preceded by 4 or 25% bovine serum albumin (BSA), 4 or 25% dextran (Dx), or homologous plasma. Saline expansion led to a two- to four-fold increase in arterial plasma ANF level in all five protocols. Both 4 and 25% BSA caused no or very modest increase in plasma ANF, while all other colloid expanders caused the expected ANF release. In all protocols, plasma ANF closely correlated with central venous pressure (CVP). BSA expansion was the only protocol with no correlation between PV and ANF release. Changes in serum Ca2+ could not explain this finding. During BSA expansion, the lack of atrial response was related to the absence of increment (or even fall) in CVP despite the expanded PV. Similarly, urinary Na+ excretion was correlated both with CVP and ANF level but not with PV in BSA expansion. When the dogs were depleted of histamine before BSA infusion, the atrial secretory response was restored, suggesting that this colloid was associated with augmented capillary leakiness and vascular fluid efflux. These results show that the expansion of PV leads neither to ANF release nor to Na+ excretion if it is not accompanied by an expanded central blood volume with elevated atrial pressure.Key words: atrial natriuretic factor, volume expansion, isotonic saline, bovine serum albumin, dextran, homologous plasma.

Isotonic saline causes greater volume overload than electrolyte-free irrigating fluids

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Robert G. Hahn
Keyword(s):  
Urinary Excretion ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Volume Overload ◽  
Systemic Absorption ◽  
Free Fluid ◽  
Plasma Volume Expansion ◽  
Pooled Data ◽  
Elimination Half

Abstract Objectives Systemic absorption of the irrigating fluid used to flush the operating site is a potentially serious complication in several types of endoscopic operations. To increase safety, many surgeons have changed from a monopolar to a bipolar resection technique because 0.9% saline can then be used instead of electrolyte-free fluid for irrigation. The present study examines whether the tendency for excessive plasma volume expansion is greater with saline than with electrolyte-free fluid. Methods Pooled data were analyzed from four studies in which a mean of 1.25 L of either 0.9% saline or an electrolyte-free irrigating fluid containing glycine, mannitol, and sorbitol was given by intravenous infusion on 80 occasions to male volunteers and patients scheduled for transurethral prostatic surgery. The distribution of the infused fluid was analyzed with a population volume kinetic model based on frequently measured hemodilution and the urinary excretion. Results Electrolyte-free fluid distributed almost twice as fast and was excreted four times faster than 0.9% saline. The distribution half-life was 6.5 and 10.6 min for the electrolyte-free fluid and saline, respectively, and the elimination half-lives (by urinary excretion) from the plasma volume were 21 and 87 min. Simulation showed that the plasma volume expansion was twice as great from 0.9% saline than from electrolyte-free fluid. Conclusions Isotonic (0.9%) saline expands the plasma volume by twice as much as occurs with electrolyte-free irrigating fluids. This difference might explain why signs of cardiovascular overload are the most commonly observed adverse effects when saline is absorbed during endoscopic surgery.

Effects of a three-day head-down tilt on renal and hormonal responses to acute volume expansion

1999 ◽  
Vol 277 (5) ◽  
pp. R1444-R1452 ◽  
Author(s):  
Pierre Mauran ◽  
Saïd Sediame ◽  
Anne Pavy-Le Traon ◽  
Alain Maillet ◽  
Alain Carayon ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Upright Position ◽  
Hormonal Responses ◽  
Water Load ◽  
Time Control ◽  
Supine Posture ◽  
Baseline Values

To clarify whether exposure to 6° head-down tilt (HDT) leads to alterations in body fluid volumes and responses to a saline load similar to those observed during space flight we investigated eight healthy subjects during a 4-day, 6° HDT and during a time-control ambulatory period with cross-over. Compared with the ambulatory period, HDT was associated with greater urinary excretion of water and sodium (UV, UNaV) from 0 to 12 h (cumulated UV 1,781 ± 154 vs. 1,383 ± 170 ml, P < 0.05; cumulated UNaV 156 ± 14 vs. 117 ± 9 mmol, P < 0.05), and with higher plasma atrial natriuretic factor (ANF) at 4 h. Hemoglobin and hematocrit increased over the first 24 h, and blood and plasma volumes were decreased after 48 h of HDT ( P< 0.05). Plasma renin activity (PRA) and aldosterone did not differ between the two groups. With prolongation of HDT, UV and UNaV returned close to baseline values. On the fourth HDT day, a 30-min infusion of 20 ml/kg isotonic saline was performed, while a large oral water load maintained a high urine output. The ambulatory period experiment was done with the subjects in the acute supine posture. Sodium excreted within 4 h of loading was 123 ± 8 mmol during HDT vs. 168 ± 16 mmol during the ambulatory period ( P < 0.05). The increase in plasma ANF and decrease in PRA were greater during HDT than during the ambulatory period (ANF 30 ± 5 vs. 13 ± 4 pg/ml, P < 0.05; PRA −1.4 ± 0.4 vs. −0.5 ± 0.2 ng ⋅ ml−1 ⋅ h−1, P < 0.05). Our data suggest that after a 3-day HDT period, thoracic volume receptor loading returns to the level seen in the upright position, leading to blunted responses to volume expansion, compared with acute supine control.

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