Pre- or post-treatment with aminoguanidine attenuates a renal distal acidification defect induced by acute ureteral obstruction in rats

2013 ◽  
Vol 91 (11) ◽  
pp. 920-928 ◽  
Author(s):  
S. Mostafa Moosavi ◽  
Zohreh Bagheri ◽  
Izadpanah Gheitasi ◽  
Jamshid Roozbeh
Keyword(s):  
Ureteral Obstruction ◽  
Left Kidney ◽  
Free Water ◽  
Urine Osmolality ◽  
Treated Group ◽  
Post Treatment ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Inos Inhibitor

Acute unilateral ureteral obstruction (UUO) impairs distal nephron acid secretion and stimulates expression of inducible nitric oxide synthase (iNOS) in post-obstructed kidney (POK). This study investigated the influence of pre- or post-treatment with aminoguanidine as a selective iNOS inhibitor on UUO-induced renal functional disturbances. To induce acute UUO, the left ureter in rats was ligated and released after 24 h. Then, a 3 h clearance period followed by bicarbonate loading and thereafter a 30 min clearance period were allocated. Aminoguanidine was administered either prior to the UUO induction or after release of the obstruction in the different rat groups, while untreated and sham groups received normal saline. During the first clearance period, fractional bicarbonate excretion and urinary pH increased markedly in the POK of the untreated group compared with the left kidney of sham group, and a large drop in the difference between urine and blood pCO2 (U–B pCO2) was observed after bicarbonate loading; all of these parameters were ameliorated in the pre-treated and post-treated groups. However, the UUO-induced decreases in creatinine clearance, sodium reabsorption, urine osmolality, and free-water reabsorption in the POK were attenuated only in the post-treated group. Therefore, the in vivo application of a selective iNOS inhibitor partially improved the acute UUO-induced distal nephron acidification defect, while post-treatment but not pre-treatment with aminoguanidine ameliorated decrements of glomerular filtration, sodium reabsorption, and urine-concentrating ability.

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Mechanisms of the antinatriuretic action of physiological doses of angiotensin II in man

1989 ◽  
Vol 76 (6) ◽  
pp. 653-658 ◽  
Author(s):  
Peter H. Seidelin ◽  
John J. McMurray ◽  
Allan D. Struthers
Keyword(s):  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Distal Nephron ◽  
Aldosterone Secretion ◽  
Significant Fall ◽  
Parallel Change ◽  
Proximal Tubular

1. Angiotensin 11 (ANG II; 1 ng min−1 kg−1) or 5% (w/v) d-glucose (placebo) was infused in six normal male volunteers, pretreated with 500 mg of lithium carbonate, who were undergoing maximal water diuresis. 2. This dose of ANG II caused a circulating increment within the physiological range (27 ± 4 to 48 ± 9 pmol/l). 3. Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 ± 13 to 82 ± 10 μmol/min). This antinatriuretic effect occurred without a fall in creatinine clearance (107 ± 3 versus 113 ± 3 ml/min). 4. ANG II caused a significant fall in fractional lithium clearance (28 ± 2 to 23 ± 2%). This may indicate a proximal tubular effect of ANG II. 5. ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. A parallel change in these two separate markers of proximal function supports an action of ANG II at this nephron segment. 6. Furthermore, the antinatriuretic effect of ANG II was unlikely to be due to stimulation of aldosterone secretion because (a) the fall in sodium excretion was temporally dissociated from the rise in aldosterone secretion, (b) potassium excretion also tended to fall during ANG II infusion and (c) aldosterone has a distal nephron effect, while, in this study, proximal nephron fractional reabsorption of sodium increased and distal nephron fractional reabsorption of sodium was unchanged. 7. These observations suggest that physiological increments in ANG II can have an antinatriuretic effect in man, which, at least initially, results from increased proximal tubular sodium reabsorption and is independent of the effect of aldosterone.

Distal tubular electrolyte transport during inhibition of renal 11β-hydroxysteroid dehydrogenase

2001 ◽  
Vol 280 (1) ◽  
pp. F172-F179 ◽  
Author(s):  
Katharine J. Biller ◽  
Robert J. Unwin ◽  
David G. Shirley
Keyword(s):  
Distal Tubule ◽  
Hydroxysteroid Dehydrogenase ◽  
Treated Group ◽  
High Dose ◽  
Mineralocorticoid Receptors ◽  
Distal Nephron ◽  
Collecting Ducts ◽  
Micropuncture Study ◽  
Stimulation Of

To test the proposal that the enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) confers aldosterone specificity on mineralocorticoid receptors in the distal nephron by inactivating glucocorticoids, we performed a free-flow micropuncture study of distal tubular function in adrenalectomized rats infused with high-dose corticosterone. One-half of the rats were additionally given intravenous carbenoxolone (CBX; 6 mg/h) to inhibit renal 11β-HSD activity. Although this maneuver lowered fractional Na+ excretion (1.1 ± 0.2 vs. 1.9 ± 0.2%, P < 0.01), Na+ reabsorption within the accessible distal tubule was found to be similar in the two groups of animals. In contrast, distal tubular K+ secretion was enhanced in CBX-treated rats: fractional K+ deliveries to the early and late distal collection sites in the corticosterone-alone group were 13 ± 1 and 20 ± 3%, respectively (not significant), whereas corresponding data in the CBX-treated group were 9 ± 1 and 24 ± 2% ( P < 0.01). This stimulation of distal K+ secretion provides the first direct in vivo evidence that 11β-HSD normally prevents corticosterone from exerting a mineralocorticoid-like effect in the distal tubule. The reduction in fractional Na+ excretion during inhibition of 11β-HSD, in the absence of a change in end-distal Na+delivery, suggests enhanced Na+ reabsorption in the collecting ducts.

Effect of calcitonin on urine concentration in the rat

1983 ◽  
Vol 244 (4) ◽  
pp. F432-F435 ◽  
Author(s):  
S. Carney ◽  
T. Morgan ◽  
C. Ray ◽  
L. Thompson
Keyword(s):  
Water Permeability ◽  
Partial Agonist ◽  
Collecting Duct ◽  
Free Water ◽  
Urine Concentration ◽  
Distal Nephron ◽  
Free Water Clearance ◽  
Normal Increase

Because mammalian distal nephron segments with both calcitonin- and antidiuretic hormone- (ADH) sensitive adenylate cyclase activity have been described, in vivo and in vitro experiments were performed to study the effect of calcitonin on rat distal nephron water permeability. Calcitonin 1 and 0.1 U/ml, but not 0.01 U/ml, significantly increased the diffusional water permeability in the isolated papillary collecting duct by 15 and 11%, respectively. However, this effect was small when compared with a 68% increase with a supramaximal concentration of ADH (from 4.0 +/- 0.3 to 6.7 +/- 0.9 microns/s; n = 6, P less than 0.01). The normal increase in water permeability with increasing concentration of ADH (0.02 and 0.2 mU/ml) was depressed by the previous addition of calcitonin (1 U/ml) to the bath but was unaltered with the supramaximal ADH concentration (2 mU/ml). Verapamil, a compound that antagonizes cellular calcium entry, did not alter the effect of calcitonin on diffusional water permeability. Calcitonin in concentrations of 0.05, 0.5, and 5 U/ml produced a significant reduction in urine flow and free water clearance. Pretreatment with calcitonin in these concentrations inhibited the antidiuretic action of ADH. These studies suggest that calcitonin acts as a partial agonist to ADH within the distal nephron. It is unclear whether such an action represents a physiological or a pharmacological effect.

scholarly journals ANP-mediated inhibition of distal nephron fractional sodium reabsorption in wild-type and mice overexpressing natriuretic peptide receptor

2010 ◽  
Vol 298 (1) ◽  
pp. F103-F108 ◽  
Author(s):  
Di Zhao ◽  
Kailash N. Pandey ◽  
L. Gabriel Navar
Keyword(s):  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Natriuretic Peptide Receptor ◽  
Distal Nephron ◽  
Peptide Receptor ◽  
Natriuretic Peptide Receptor A ◽  
Npr1 Gene

Atrial natriuretic peptide (ANP) elicits natriuresis; however, the relative contributions of proximal and distal nephron segments to the overall ANP-induced natriuresis have remained uncertain. This study was performed to characterize the effects of ANP on distal nephron sodium reabsorption determined after blockade of the two major distal nephron sodium transporters with amiloride (5 μg/g body wt) plus bendroflumethiazide (12 μg/g body wt) in male anesthetized C57/BL6 and natriuretic peptide receptor-A gene (Npr1) targeted four-copy mice. The lower dose of ANP (0.1 ng·g body wt−1·min−1, n = 6) increased distal sodium delivery (DSD, 2.4 ± 0.4 vs. 1.6 ± 0.2 μeq/min, P < 0.05) but did not change fractional reabsorption of DSD compared with control (86.3 ± 2.0 vs. 83.9 ± 3.6%, P > 0.05), thus limiting the magnitude of the natriuresis. In contrast, the higher dose (0.2 ng·g body wt−1·min−1, n = 6) increased DSD (2.8 ± 0.3 μeq/min, P < 0.01) and also decreased fractional reabsorption of DSD (67.4 ± 4.5%, P < 0.01), which markedly augmented the natriuresis. In Npr1 gene-duplicated four-copy mice ( n = 6), the lower dose of ANP increased urinary sodium excretion (0.6 ± 0.1 vs. 0.3 ± 0.1 μeq/min, P < 0.05) and decreased fractional reabsorption of DSD compared with control (72.2 ± 3.4%, P < 0.05) at similar mean arterial pressures (91 ± 6 vs. 92 ± 3 mmHg, P > 0.05). These results provide in vivo evidence that ANP-mediated increases in DSD alone exert modest effects on sodium excretion and that inhibition of fractional reabsorption of distal sodium delivery is requisite for the augmented natriuresis in response to the higher dose of ANP or in Npr1 gene-duplicated mice.

Effect of acetylcholine, atropine, and physostigmine on renal function in the dog

1964 ◽  
Vol 206 (3) ◽  
pp. 492-498 ◽  
Author(s):  
Arthur J. Vander
Keyword(s):  
Renal Artery ◽  
Renal Plasma Flow ◽  
Left Kidney ◽  
Urine Volume ◽  
Indirect Evidence ◽  
Urine Osmolality ◽  
Sodium Concentration ◽  
Sodium Reabsorption ◽  
Left Renal Artery ◽  
Parasympathetic Innervation

Acetylcholine (1–500 µg/min), atropine (.002–.12 mg/kg min), or physostigmine (.01–.08 mg/min) was infused directly into the left renal artery of anesthetized dogs, and right and left kidney functions were compared. Acetylcholine produced variable changes in glomerular filtration rate (–30 to +55%), but always increased renal plasma flow (4–115%), sodium excretion (20–365 µm/min), potassium excretion (1–56 µm/min), and urine volume (.25–3.1 ml/min). Filtration fraction, urine osmolality, and medullary sodium concentration were always reduced. These changes could all be reversed or prevented by atropine. Stop-flow studies failed to demonstrate any distal tubular inhibition of sodium reabsorption by acetylcholine. Neither atropine nor physostigmine, when infused into the renal artery by itself, produced any changes in renal hemodynamics or electrolyte excretion. These data demonstrate that acetylcholine can decrease renal arteriolar resistance and inhibit tubular sodium reabsorption. They also provide indirect evidence which supports, but does not prove, the hypothesis that the kidney lacks parasympathetic innervation.

scholarly journals Distribution of selenium in sheep treated with dipheny diselenide

2018 ◽  
Vol 70 (4) ◽  
pp. 1017-1022
Author(s):  
M.L.R. Leal ◽  
J.B.T. Rocha ◽  
C.L.D. Corte ◽  
A.R. Aires ◽  
J.F.X. Rocha ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Single Dose ◽  
Intravenous Injection ◽  
Selenium Concentration ◽  
Treated Group ◽  
Post Treatment ◽  
Control Group ◽  
Diphenyl Diselenide ◽  
Single Intravenous Injection

ABSTRACT The aim of the present study was to report the in vivo distribution of selenium in sheep. For this, animals were allocated into two groups (control group and treated group) and kept in metabolic cages for a period of 37 days. The treated group received a single dose (6µmol/kg) of Diphenyl Diselenide, intravenously. Plasma and erythrocytes samples were collected at different times. Adipose tissue, muscles (latissimusdorsi, semitendinosus, and supra-scapular) heart, liver, lung, kidney, intestine and brain were sampled at 30 days post-treatment, in order to determine the selenium concentration. The results demonstrated that the selenium, from the Diphenyl Diselenide group, was higher in erythrocytes (4.8mg/L, six hours post-treatment) when compared with the control sheep. The deposition of selenium occurred in the liver (7.01µg/g), brain (3.53µg/g) and kidney (2.02µg/g). After 30 days of a single intravenous injection of Diphenyl Diselenide, liver was the main organ of selenium deposition.

scholarly journals Blockade of renal medullary bradykinin B2 receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

2008 ◽  
Vol 295 (3) ◽  
pp. F811-F817 ◽  
Author(s):  
Sema-Hayriye Sivritas ◽  
David W. Ploth ◽  
Wayne R. Fitzgibbon
Keyword(s):  
Blood Flow ◽  
Left Kidney ◽  
Treated Group ◽  
Control Group ◽  
Sodium Reabsorption ◽  
Salt Diet ◽  
Excretory Function ◽  
Time Control ◽  
Medullary Blood Flow ◽  
Hoe 140

The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B2 (BKB2) receptors to acutely increase papillary blood flow (PBF) and therefore Na+ excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB2 receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)- or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 μg·kg−1·h−1, treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na+ excretion (urinary Na+ extraction rate) and fractional Na+ excretion by 40 ± 5% and 40 ± 4%, respectively ( P < 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB2 receptors to increase Na+ excretion independent of changes in inner medullary blood flow.

Effect of Inhibition of Prostaglandin Synthesis on the Natriuresis Induced by Saline Infusion in Man

1978 ◽  
Vol 54 (1) ◽  
pp. 47-50 ◽  
Author(s):  
Th. Mountokalakis ◽  
Th. Karambasis ◽  
D. Mayopoulousymvoulidou ◽  
G. Merikas
Keyword(s):  
Free Water ◽  
Prostaglandin Synthesis ◽  
Saline Infusion ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Prostaglandin Synthetase ◽  
Water Reabsorption ◽  
Post Infusion ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Natriuretic Effect

1. The effect of oral administration of an inhibitor of prostaglandin synthetase, indomethacin, on the natriuresis induced by the infusion of sodium chloride (saline) was studied in 11 healthy volunteers. 2. The administration of indomethacin did not alter sodium excretion before saline infusion, but it resulted in a significant increase of the natriuresis after saline infusion. This increase was not accompanied by any change in post-infusion urine flow rate or free water reabsorption. 3. It is suggested that intrarenal prostaglandins might suppress the natriuretic effect of saline infusion, probably by increasing sodium reabsorption in the distal nephron.

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