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.

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.

Influence of Volume Expansion on Renal Diluting Capacity in the Rat

1974 ◽  
Vol 46 (3) ◽  
pp. 331-345
Author(s):  
M. Martinez-Maldonado ◽  
G. Eknoyan ◽  
W. N. Suki
Keyword(s):  
Volume Expansion ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Free Water ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Water Excretion ◽  
Hypotonic Saline

1. The functional capacity of Henle's loop was examined during hypotonic, isotonic and hypertonic extracellular fluid volume expansion. To eliminate a possible role of antidiuretic hormone (ADH) in the alteration of free water excretion, rats with congenital diabetes insipidus were used. The infusion of hypotonic saline resulted in a progressive rise in free water clearance (CH2O) throughout the range of urine flow (V) attained. Similar results were obtained in rats treated chronically with deoxycorticosterone acetate (DOCA). The infusion of isotonic saline (sodium chloride, 154 mmol/l) produced an initial rise in CH2O until V represented 10% of the filtered load, after which CH2O appeared to reach a plateau. The limitation of CH2O was more marked when hypertonic saline was infused. Medullary and papillary non-urea solute (NUS) concentration rose progressively with the increasing concentration of the saline solution infused. 2. The greater fractional sodium excretion (FENa) after acute isotonic and hypertonic volume expansion is probably the result of inhibition of sodium reabsorption in the collecting duct, although inhibition in the ascending limb cannot be entirely excluded. The depression of CH2O as a function of V seen during acute isotonic or hypertonic volume expansion can be attributed in part to enhanced water back-diffusion from the collecting duct consequent to the increasing medullary and papillary interstitial NUS concentration, even in the absence of ADH. 3. Chronic expansion of extracellular fluid volume by DOCA administration did not modify the response to hypotonic saline infusion.

Abstract P147: Attenuation Of Diuretic And Natriuretic Responses To Acute Saline Volume Expansion In Mice Pre-treated With Tumor Necrosis Factor-alpha (TNFα) Inhibitor, Etanercept.

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Dewan S Majid ◽  
Alexander Castillo
Keyword(s):  
Intravenous Infusion ◽  
Volume Expansion ◽  
Salt Intake ◽  
Isotonic Saline ◽  
Physiological Role ◽  
Baseline Period ◽  
Sodium Reabsorption ◽  
High Salt Intake ◽  
Intravenous Saline ◽  
Tnfα Inhibitor

High salt intake induces an immune response that activates the mononuclear phagocyte system (MPS) cells to produce TNFα. We have previously demonstrated that intravenous infusion of TNFα in mice induces diuresis and natriuresis by inhibiting renal tubular sodium reabsorption. We hypothesize that the intravenous saline infusion can also induce the production of TNFα from MPS cells and such increase in TNFα influences saline induced natriuresis in the kidney. To examine this hypothesis, we measured the changes in TNFα levels in plasma and in urinary excretion rate (U TNFα V) during intravenous infusion of isotonic saline (0.9% NaCl), first at euvolemic condition (3 μL/min for 60 min; Baseline period) and then at an enhanced infusion rate (12 μL/min for 90 min; Volume expansion period) in anesthetized mice (n=5). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by PAH and inulin clearances respectively. TNFα concentration in plasma and urine samples were determined using ELISA kit (Ebioscience, Woburn, MA). TNFα level in plasma collected during baseline period was undetectable, however, TNFα was increased to 3.7±1.3 pg/mL during volume expansion (VE) period. Baseline U TNFα V level was 0.01±0.002 pg/min/g (kidney wt), which was increased to 0.11±0.03 pg/min/g (P<0.05) during VE period. VE increased urine flow (V, 5.4±0.5 to 22.0±5.1 μL/min/g; P<0.05) and sodium excretion (U Na V; 0.54±0.19 to 4.84 ±1.16 μmol/min/g; P<0.05) without significant changes in RBF (7.1±1.0 to 6.0±1.8 mL/min/g) and GFR (1.18±0.11 to 0.94±0.28 mL/min/g). Interestingly, the diuretic and natriuretic responses to VE were markedly attenuated in mice (n=5) pretreated with a TNFα inhibitor, etanercept (ETN; 0.5 mg/kg intraperitoneally once daily for 3 days prior to the experiment day). VE induced changes in ETN treated mice are as follows: V, 5.9±0.65 to 7.9 ±1.6 μL/min/g; U Na V, 0.43±0.6 to 1.1±0.28 μmol/min/g; RBF, 5.4±0.4 to 6.6±0.9 mL/min/g and GFR, 0.87±0.09 to 0.98±0.13 mL/min/g. These findings demonstrate for the first time that an intravenous saline volume infusion resulted an increase in TNFα level in plasma and in urine. These results strongly suggest a physiological role for TNFα in regulating renal excretory function during saline volume expansion.

Interactions between angiotensin and nitric oxide in the renal response to volume expansion

1995 ◽  
Vol 269 (3) ◽  
pp. R504-R510 ◽  
Author(s):  
M. T. Llinas ◽  
J. D. Gonzalez ◽  
F. J. Salazar
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibition ◽  
Renal Response ◽  
Group 2 ◽  
Extracellular Volume Expansion

This study examined, in anesthetized dogs, the possible interactions between nitric oxide (NO) and angiotensin II (ANG II) in mediating the renal response to an extracellular volume expansion (ECVE). It was found that the intrarenal maintenance of ANG II levels (group 1) or the intrarenal NO synthesis inhibition (group 2) did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional lithium excretion (FeLi). In the third group, ANG II synthesis was inhibited during NO synthesis blockade. It was found in this group that the NO synthesis inhibition reduced the ECVE-induced increment in sodium excretion (P < 0.05) but did not modify the ECVE-induced increment in FeLi. These results suggest that the increase of proximal sodium reabsorption induced by the No synthesis inhibition is mediated by endogenous ANG II levels. In the fourth group, it was observed that NO synthesis inhibition, during the intrarenal maintenance of ANG II levels, induced a decrease of renal blood flow (P < 0.05) and reduced the natriuretic response to ECVE to a lower level (P < 0.05) than that observed in groups 1 and 2. The results of this group suggest that endogenous NO modulates the vasoconstrictor and antinatriuretic effects of ANG II during an ECVE. In summary, the results of this study suggest that there is an important interaction between NO and ANG II in mediating the renal response to an ECVE.

Renal sodium reabsorption following induction of recovery from volume expansion

1977 ◽  
Vol 233 (5) ◽  
pp. F416-F420
Author(s):  
T. F. Knight ◽  
E. J. Weinman
Keyword(s):  
Urinary Excretion ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Recovery Phase ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Renal Sodium Reabsorption ◽  
Distal Delivery

In the rat, infusion of a volume of isotonic saline equal to 2% of body weight resulted in an 82% increase in delivery of filtrate out of the proximal tubule but little or, in some animals, no change in the urinary excretion of sodium. By contrast, further degrees of volume expansion resulted in lesser increases in the distal delivery of filtrate, but were associated with a marked increase in the urinary excretion of sodium. Sixty minutes following completion of volume expansion, while the animals were still in positive sosium balance, the urinary excretion of sodium decreased 52% compared to a decrease of only 24% in the distal delivery of filtrate. During the course of progressive volume expansion and during the recovery phase, there was a dissociation between alterations in sodium reabosrption in the proximal convoluted tubule and in the whole kidney. These studies indicate that although the proximal tubule is more sensitive to changes in the extracellular fluid volume, distal nephron sites are ultimately responsible both for the natriuresis of volume expansion and the relative antinatriuresis of the recovery periods.

Role of intrarenal angiotensin II in mediating renal response to volume expansion

1991 ◽  
Vol 261 (3) ◽  
pp. R619-R625 ◽  
Author(s):  
J. M. Pinilla ◽  
M. C. Perez ◽  
I. Hernandez ◽  
T. Quesada ◽  
J. Garcia-Estan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Relative Role ◽  
Ang Ii ◽  
Renal Response ◽  
The Right

Natriuresis induced by extracellular volume expansion (ECVE) is accompanied by a decrease in renin release and by an increase of renal interstitial hydrostatic pressure (RIHP). This study was undertaken to examine, in anesthetized dogs, the relative role of intrarenal angiotensin II (ANG II) changes in mediating natriuresis, diuresis, and increases in RIHP induced by two different levels of volume expansion (1.5 and 5% body wt in 45 min) with isotonic saline. Intrarenal ANG II levels were maintained in the right kidney throughout the experiment by simultaneously infusing captopril (0.8 micrograms.kg-1.min-1) and ANG II (1 ng.kg-1.min-1) into the right renal artery. In response to 5% ECVE, increases in RIHP, natriuresis, and diuresis were inhibited in the right kidney by 55, 40, and 47% respectively, when compared with the left kidney. Significant increases occurred in plasma atrial natriuretic peptide (ANP) levels during 5% ECVE. Maintenance of constant intrarenal ANG II levels during 1.5% ECVE completely abolished the increment of RIHP and diuresis and inhibited the natriuretic response by 80% in the right kidney when compared with the left kidney. Plasma ANP levels did not change during the 1.5% ECVE. No differences between kidneys were found when the intrarenal effects of ANG II were blocked with saralasin before saline loading. These results suggest that increases in RIHP, natriuresis, and diuresis during ECVE are partially mediated by decreases in intrarenal ANG II levels. Furthermore, these results indicate that the role of intrarenal ANG II levels in mediating the renal response to ECVE is more important when plasma ANP levels do not change than when they are increased.

scholarly journals mPGES-1 deletion impairs diuretic response to acute water loading

2009 ◽  
Vol 296 (5) ◽  
pp. F1129-F1135 ◽  
Author(s):  
Sunhapas Soodvilai ◽  
Zhanjun Jia ◽  
Mong-Heng Wang ◽  
Zheng Dong ◽  
Tianxin Yang
Keyword(s):  
Prostaglandin E ◽  
Wild Type ◽  
Prostaglandin E Synthase ◽  
Water Load ◽  
Water Loading ◽  
Water Handling ◽  
Diuretic Response ◽  
Established Role ◽  
Stimulation Of

PGE2 has an established role in renal water handling. The present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1) in the diuretic response to acute and chronic water loading. Compared with wild-type (+/+) controls, mPGES-1 −/− mice exhibited impaired ability to excrete an acute, but not chronic water load. In response to acute water loading, urinary PGE2 excretion in the +/+ mice increased at 2 h, in parallel with increased urine flow. In contrast, the −/− mice exhibited a delayed increase in urinary PGE2 excretion, coinciding with the stimulation of renal medullary mRNA expression of cytosolic prostaglandin E synthase but not mPGES-2. At baseline, renal aquaporin-2 (AQP2) expression in mPGES-1 −/− mice was enhanced compared with the +/+ control. In response to acute water loading, renal AQP2 expression in the +/+ mice was significantly reduced, and this reduction was blunted in the −/− mice. Despite striking changes in AQP2 protein expression, renal AQP2 mRNA in both genotypes largely remained unchanged. Overall, these data support an important role of mPGES-1 in provoking the diuretic response to acute water loading.

Role of prostaglandins on the renal effects of angiotensin and interstitial pressure during volume expansion

1993 ◽  
Vol 265 (6) ◽  
pp. R1469-R1474 ◽  
Author(s):  
J. M. Pinilla ◽  
A. Alberola ◽  
J. D. Gonzalez ◽  
T. Quesada ◽  
F. J. Salazar
Keyword(s):  
Volume Expansion ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibitor ◽  
Extracellular Volume Expansion ◽  
The Right

This study was undertaken to determine, in anesthetized dogs, the role of renal prostaglandins (PG) in mediating the natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during extracellular volume expansion (ECVE) with isotonic saline. It was also determined if the intrarenal angiotensin II (ANG II) effects during ECVE are potentiated by the inhibition of PG synthesis. ECVE induced similar elevations of RIHP, natriuresis, and fractional lithium excretion in dogs treated (n = 7) and not treated with a PG synthesis inhibitor (n = 5). In other experimental groups, the effects of the intrarenal maintenance of ANG II levels (n = 6) by infusing captopril and ANG II into the right renal artery were compared with those induced by the simultaneous infusion of captopril, ANG II, and a PG synthesis inhibitor (n = 6). In response to ECVE, renal blood flow and glomerular filtration rate were similar in both kidneys when ANG II levels were maintained constant and were significantly higher in the left kidney when ANG II levels were maintained constant and PG synthesis was inhibited in the right kidney. However, when compared with the left kidney, the ECVE-induced increments of natriuresis and RIHP in the right kidney were reduced by the same magnitude when intrarenal ANG II was maintained constant with (36 and 53%, respectively) and without (40 and 54%, respectively) the simultaneous PG synthesis inhibition. Our results indicate that during ECVE, renal PGs do not play an important role in mediating the RIHP-induced increments in natriuresis and decrements in proximal sodium reabsorption. (ABSTRACT TRUNCATED AT 250 WORDS)

Development of the renal response to blood volume expansion in normal and fast-growing rats

1976 ◽  
Vol 231 (3) ◽  
pp. 832-836
Author(s):  
HH Bengele ◽  
S Solomon
Keyword(s):  
Volume Expansion ◽  
Control Period ◽  
Male Rats ◽  
Regulatory Function ◽  
Chronological Age ◽  
Donor Blood ◽  
Fast Growing ◽  
Growing Rats ◽  
Blood Volume Expansion ◽  
Diuretic Response

Male rats from reduced (fast-growing) litters between 14 and 50 days of age were studied. Standard renal clearnce techniques were employed. After a 60-min control period, the animals were infused (2.3% body wt) with heparinized donor blood obtained from lillermates of the same age. Renal function was followed for an additional 60 min. The efficiency of the diuretic response, the percent infused volume excreted above control levels, and the sodium efficiency, the percent infused Na excreted, were calculated. Results indicate that both efficiencies develop in a discontinuous pattern and that they are comparable. This pattern of development, as well as the magnitude of the mature response, is comparable to that previously reported for rats from intact (normally growing) litters. The onset and attainment of the mature response is, however, shifted in time, such that reduced-litter animals achieve the mature response 10-15 days earlier than intact-litter rats. Results exclude chronological age or body weight alone as principal determinant of the mature response and suggest that some function of growth rate is responsible for the maturation of this regulatory function.

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

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