Vascular sensitivity to prostaglandin I2 and urinary excretion of 6-keto-prostaglandin F1α in conscious dogs

1986 ◽  
Vol 71 (5) ◽  
pp. 527-532 ◽  
Author(s):  
Robert L. Jones ◽  
Michael L. Watson
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Sodium Excretion ◽  
Hydrolysis Product ◽  
Urinary Sodium Excretion ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Gas Chromatography Mass Spectrometry ◽  
Prostaglandin I2 ◽  
Stable Isotope Dilution

1. A method is described for measuring the urinary excretion of 6-keto-prostaglandin F1α, the stable hydrolysis product of prostaglandin I2, by stable isotope dilution gas chromatography–mass spectrometry. 2. Three different doses of prostaglandin I2 were infused intravenously into conscious dogs and the effects on systemic and renal haemodynamics and urinary sodium excretion were observed. 3. The two highest infusion rates of prostaglandin I2 (15 and 30 ng min−1 kg−1 body weight) induced significant decreases in systematic blood pressure and dose-related increases in sodium excretion, but no change in renal haemodynamics. 4. There was a linear relationship between urinary excretion of 6-keto-prostaglandin F1α and the rate of infusion of prostaglandin I2. 5. The calculated basal rate of entry of prostaglandin I2 into the systematic circulation in conscious dogs is 4 ng min−1 kg−1 body weight, which is substantially higher than that previously reported in man.

Rhythmicity of urinary sodium excretion, mean arterial blood pressure, and heart rate in conscious dogs

1992 ◽  
Vol 262 (1) ◽  
pp. H149-H156 ◽  
Author(s):  
U. Palm ◽  
W. Boemke ◽  
H. W. Reinhardt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
Infusion Regimen

The existence of urinary excretion rhythms in dogs, which is a matter of controversy, was investigated under strictly controlled intake and environmental conditions. In seven conscious dogs, 14.5 mmol Na, 3.55 mmol K, and 91 ml H2O.kg body wt-1.24 h-1 were either administered with food at 8:30 A.M. or were continuously infused at 2 consecutive days. During these 3 days, automatized 20-min urine collections, mean arterial blood pressure (MABP), and heart rate (HR) recordings were performed without disturbing the dogs. Fundamental and partial periodicities, the noise component of urinary sodium excretion (UNaV), MABP, and HR were analyzed using a method derived from Fourier and Cosinor analysis. Oral intake (OI) leads to powerful 24-h periodicities in all dogs and seems to synchronize UNaV. UNaV on OI peaked between 1 and 3 P.M. Under the infusion regimen, signs of nonstationary rhythms and desynchronization predominated. UNaV under the infusion regimen could be separated into two components: a rather constant component continuously excreted and superimposed to this an oscillating component. No direct coupling between UNaV and MABP periodicities could be demonstrated. On OI, an increase in HR seems to advance the peak UNaV in the postprandial period. HR and MABP signals were both superimposed with noise. We conclude that UNaV rhythms are present in dogs. They are considerably more pronounced on OI.

Postprandial natriuresis in humans: further evidence that urodilatin, not ANP, modulates sodium excretion

1996 ◽  
Vol 270 (2) ◽  
pp. F301-F310 ◽  
Author(s):  
C. Drummer ◽  
W. Franck ◽  
M. Heer ◽  
W. G. Forssmann ◽  
R. Gerzer ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Salt ◽  
Peak Rate ◽  
High Salt Intake ◽  
Low Salt ◽  
Chloride Excretion

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mumol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary excretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/min. The effect of high-salt intake on urinary sodium, chloride, and urodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin and sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which was acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriuretic profile, and no positive correlation between plasma ANP and sodium excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily involved in the regulation of the excretion of sodium and chloride.

Failure of renal denervation to attenuate hypertension in Dahl NaCl-sensitive rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2428-2432 ◽  
Author(s):  
J. Michael Wyss ◽  
Wanida Sripairojthikoon ◽  
Suzanne Oparil
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renal Nerves ◽  
Urinary Volume ◽  
Volume Output

In previous experiments we have demonstrated that the renal nerves play a significant role in all genetic and (or) induced models of hypertension that we have studied. The current experiments extended this research by investigating the contribution of the renal nerves to hypertension in the Dahl NaCl-sensitive rat. This was investigated by assessing the effect of bilateral phenol renal denervation carried out prior to initiation of a high NaCl (8% NaCl) diet. In two separate studies, renal denervation did not affect systolic blood pressure in either Dahl NaCl-sensitive rats or their normotensive counterparts, Dahl NaCl-resistant rats. Further, denervation did not increase absolute urinary sodium excretion, percent urinary sodium excretion, urinary volume output, or food or water intake; nor did it differentially alter creatinine clearance or body weight. Denervation was verified at the termination of each study by a greater than 80% depletion of renal noradrenaline stores. These results indicate that the renal nerves do not provide a major contribution to hypertension in the Dahl NaCl-sensitive rat.

Role of renal arterial pressure in the regulation of extracellular volume in conscious dogs

1992 ◽  
Vol 82 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Gabriele Kaczmarczyk ◽  
Klaus Schröder ◽  
Dirk Lampe ◽  
Rainer Mohnhaupt
Keyword(s):  
Body Weight ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Central Venous ◽  
Infusion Period

1. This study in conscious dogs examined the quantitative effects of a reduction in the renal arterial pressure on the renal homoeostatic responses to an acute extracellular fluid volume expansion. 2. Seven female beagle dogs were chronically instrumented with two aortic catheters, one central venous catheter and a suprarenal aortic cuff, and were kept under standardized conditions on a constant high dietary sodium intake (14.5 mmol of Na+ day−1 kg−1 body weight). 3. After a 60 min control period, 0.9% (w/v) NaCl was infused at a rate of 1 ml min−1 kg−1 body weight for 60 min (infusion period). Two different protocols were applied during the infusion period: renal arterial pressure was maintained at 102 ± 1 mmHg by means of a servo-feedback control circuit (RAP-sc, 14 experiments) or was left free (RAP-f, 14 experiments). 4. During the infusion period, in the RAP-sc protocol as well as in the RAP-f protocol, the mean arterial pressure increased by 10 mmHg, the heart rate increased by 20 beats/min, the central venous pressure increased by 4 cmH2O and the glomerular filtration rate (control 5.1 ± 0.3 ml min−1 kg−1 body weight, mean ± sem) increased by 1 ml min−1 kg−1. 5. Plasma renin activity [control 0.85 ± 0.15 (RAP-f) and 1.08 ± 0.23 (RAP-sc) pmol of angiotensin I h−1 ml−1] decreased similarly in both protocols. 6. Renal sodium excretion, fractional sodium excretion and urine volume increased more in the RAP-f experiments than in the RAP-sc experiments (P<0.05), renal sodium excretion from 8.2 to 70.1 (RAP-f) and from 7.7 to 47.4 (RAP-sc) μmol min−1 kg−1 body weight, fractional sodium excretion from 1.1 to 8.0 (RAP-f) and from 1.0 to 5.4 (RAP-sc)% and urine volume from 39 to 586 (RAP-f) and from 38 to 471 (RAP-sc) μl min−1 kg−1 body weight. 7. In the RAP-f experiments as well as in the RAP-sc experiments, urinary sodium excretion increased with expansion of the extracellular fluid volume, which increased by a maximum of 21% (fasting extracellular fluid volume: 206 ± 4 ml/kg body weight, six dogs, 28 days). 8. The increase in renal arterial pressure contributed significantly to the renal homoeostatic response, as 21% less urine and 31% less sodium were excreted when the extracellular fluid volume was expanded and the renal arterial pressure was kept constant below control pressure rather than being allowed to rise. The differences in sodium and water excretion were mainly due to the effect of renal arterial pressure on tubular reabsorption. However, the striking increase in sodium and urine excretion which occurred despite the reduction in renal arterial pressure emphasizes the importance of other homoeostatic factors involved in body fluid regulation.

scholarly journals Increased thromboxane mediates the adverse renal effects of interleukin-2 in rats.

1994 ◽  
Vol 4 (9) ◽  
pp. 1701-1710
Author(s):  
D Rubinger ◽  
E Cohen ◽  
Y Haviv ◽  
J Bernheim ◽  
E Shiloni ◽  
...  
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Low Dose ◽  
Combined Therapy ◽  
Interleukin 2 ◽  
Chronic Administration ◽  
Urinary Sodium Excretion ◽  
Metabolic Effects ◽  
High Dose ◽  
Sodium And Potassium

The capillary leak syndrome with decreased GFR and renal water and sodium retention after recombinant interleukin-2 (IL-2) administration may arise from endothelial activation via an increase in prostaglandin synthesis. This study was undertaken to better define the role of the prostaglandin system in the renal and metabolic effects of IL-2 administration in rats. The chronic administration of IL-2 (100,000 U/kg, thrice daily, ip) resulted in a significant increase in body weight, a decrease in GFR and in the urinary excretion of sodium and potassium, and an increase in the urinary excretion of thromboxane (TXB2). After combined IL-2 and low-dose indomethacin (1.7 mg/kg per day po), a significant decrease in body weight with normalization of GFR, of the urinary excretion of Na, and of urinary TXB2 was noted in animals receiving combined therapy as compared with those receiving IL-2 alone. In contrast, high-dose indomethacin administration (33.3 mg/kg po for the last 3 days of the study) was associated with a further decrease in GFR, enhancement of the sodium and potassium retention, and suppression of prostaglandin E2 excretion. The administration of the thromboxane receptor antagonist SQ 29548 in IL-2-treated rats led to a reversal of the fall in GFR induced by the lymphokine without significant changes in urinary sodium excretion. These results support the hypothesis that thromboxane is an important mediator of the renal and systemic effects of IL-2. These effects are reversed at least partly by low-dose indomethacin, which selectively suppresses thromboxane A2 (TXA2) synthesis, or by TXA2 receptor antagonism.

Excretion of endogenous digoxin-like immunoreactive factors in human urine is a function of urine flow rate.

1988 ◽  
Vol 34 (5) ◽  
pp. 960-964 ◽  
Author(s):  
B A Siegfried ◽  
R Valdes
Keyword(s):  
Urinary Excretion ◽  
Flow Rate ◽  
Human Urine ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Healthy Humans

Abstract We studied the effect of varying water and salt intake on the renal excretion of endogenous digoxin-like immunoreactive factors (DLIF). DLIF were measured in human urine and serum by competitive displacement of 125I-labeled digoxin from anti-digoxin antibodies. Diuresis was selectively induced in normal healthy humans by acute water ingestion, and natriuresis was preferentially induced by acute saline ingestion. We found the amount of endogenous immunoreactivity excreted in urine to be correlated with urine flow rate but not with urinary sodium excretion. Urinary excretion of DLIF, normalized to creatinine, was 3.6-fold greater at a urine flow rate of 5.5 mL/min than at 0.5 mL/min. On the other hand, saline intake increased urine flow rate 1.9-fold and increased sodium excretion threefold, but did not affect urinary excretion of DLIF. Fractional excretion of DLIF was linearly related to fractional excretion of water. This study demonstrates that normalization of DLIF values to urinary creatinine does not make DLIF excretion independent of urine flow rate and underscores the need for information on urine flow rate when DLIF measurements in urine are being interpreted.

scholarly journals MO061PLASMINOGEN DEFIENCY DOES NOT PROTECT MICE FROM SODIUM RETENTION IN EXPERIMENTAL NEPHROTIC SYNDROME

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mengyun Xiao ◽  
Bernhard Nikolaus Bohnert ◽  
Matthias Woern ◽  
Edward Plow ◽  
Tobias B Huber ◽  
...  
Keyword(s):  
Body Weight ◽  
Nephrotic Syndrome ◽  
Sodium Excretion ◽  
Serine Proteases ◽  
Essential Role ◽  
Urinary Sodium Excretion ◽  
Sodium Retention ◽  
Plasmin Activity ◽  
Edema Formation

Abstract Background and Aims Sodium retention and edema formation are the hallmarks of nephrotic syndrome and thought to be mediated by proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases. Plasmin is highly abundant in nephrotic urine and has been proposed to be the principal serine protease responsible for ENaC activation in nephrotic syndrome. However, there is not enough evidence to demonstrate the essential role of plasmin in mediating sodium retention in an experimental nephrotic model. Method We investigated sodium retention and edema formation in a mouse model of nephrotic syndrome based on an inducible podocyte-specific podocin knockout (Bl6-Nphs2tm3.1Antc or Δipod * Tg(Nphs1-rtTA*3G8Jhm)* Tg(tetO-cre) 1Jaw). To generate an inducible podocin knockout with plasminogen deficient model (Nphs2Δipod * Plg-/-, hereafter referred to as Plg-/-), plasminogen deficient mice (Bl6-Plgtm1Jld or -/-) were intercrossed with Nphs2Δipod mice. Nephrotic syndrome was induced after oral doxycycline treatment for 14 days. Body weight, urinary protein, urinary sodium excretion, as well as urinary plasmin activity were daily determined 14 days after end of induction. To determine if sodium retention can be prevented by serine protease inhibitor aprotinin in Plg+/+ and Plg-/- mice after induction of nephrotic syndrome, sustained-release pellets containing aprotinin (2 mg per day) or placebo pellets were implanted to either Plg+/+ or Plg-/- mice (n=4 per group). Results Uninduced Plg+/+ (n=6-13) and Plg-/- mice (n=6-14) had normal kidney function and sodium handling. After end of doxycycline induction, there was no significant differencein proteinuria increase between Plg+/+ (from 2 ± 0 to 161 ± 16 mg/mg creatinine, p&lt;0.05) and Plg-/- mice (from 9 ± 8 to 146 ± 44 mg/mg creatinine, p&lt;0.05) leading to similar hypoalbuminemia. In urine samples from Plg+/+ mice, Western blot revealed urinary excretion of plasminogen/plasmin which was completely absent in Plg-/- mice. Accordingly, urinary plasmin activity was only detectable in Plg+/+ mice using a chromogenic substrate. After onset of proteinuria, amiloride-sensitive natriuresis was increased compared to uninduced mice indicating ENaC activation. While urinary sodium excretion dropped in both genotypes indicating sodium retention (from 193 ± 16 to 16 ± 6 µmol/24h in Plg+/+ mice, p&lt;0.05; from 229 ± 11 to 26 ± 7 µmol/24h in Plg-/-mice, p&lt;0.05). As a consequence, body weight maximum increased in both genotypes 21 ± 1% in Plg+/+ and 17 ± 2% in Plg-/- mice (p=0.616) and was paralleled by development of ascites. Urinary amidolytic activity were completely prevented by the presence of aprotinin, as well as sodium retention and ascites in both Plg+/+and Plg-/- mice. Conclusion This study shows for the first time that mice lacking urinary plasmin are not protected from ENaC-mediated sodium retention in experimental nephrotic syndrome, however it can be prevented by aprotinin. These findings point to an essential role of other hitherto unknown serine proteases excreted in nephrotic urine.

Renal Metabolism and Effects of the Glutamyl Derivatives of l-Dopa and 5-Hydroxytryptophan in Man

1996 ◽  
Vol 91 (2) ◽  
pp. 177-185 ◽  
Author(s):  
T. C. Li Kam Wa ◽  
S. Freestone ◽  
R. R. Samson ◽  
N. R. Johnston ◽  
M. R. Lee
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Competitive Inhibition ◽  
Urinary Sodium Excretion ◽  
The Other ◽  
Renal Metabolism ◽  
Dihydroxyphenylacetic Acid ◽  
Hydroxyindoleacetic Acid ◽  
Natriuretic Effect ◽  
The Given

1. Equimolar amounts of y-l-glutamyl-l-3,4-dihydroxyphenylalanine (gludopa) and γ-l-glutamyl-5-hydroxy-l-tryptophan were infused separately and together in eight healthy, salt-replete male subjects in a placebo-controlled, cross-over study to investigate whether the administration of one amine precursor affects the renal metabolism of the other and to determine whether dopamine or 5-hydroxytryptamine would be generated preferentially. The overall effect on sodium excretion was also measured when both precursors were administered simultaneously. 2. Administration of gludopa was associated with marked increases in the urinary excretion of l-dopa, dopamine and 3,4-dihydroxyphenylacetic acid, together with a rise in the urinary excretion of sodium. γ-l-Glutamyl-5-hydroxy-l-tryptophan, on the other hand, produced marked increases in the urinary excretion of 5-hydroxy-l-tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid, and this was accompanied by a slight, but non-significant, reduction in sodium excretion. About 27% of the infused dose of gludopa (on a molar basis) was recovered in the urine as dopamine whereas 15% of the given dose of γ-l-glutamyl-5-hydroxy-l-tryptophan was excreted as 5-hydroxytryptamine. 3. The urinary excretion values of l-dopa, dopamine and 3,4-dihydroxyphenylacetic acid after the simultaneous infusion of gludopa and γ-l-glutamyl-5-hydroxy-l-tryptophan were not significantly different from those observed after infusion of gludopa only. Similarly, the urinary excretion values of 5-hydroxy-l-tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid during the co-infusion were similar to those measured after administration of γ-l-glutamyl-5-hydroxy-l-tryptophan only. The net effect of the concomitant infusion of both glutamyl derivatives was an increase in urinary sodium excretion. 4. Our study in salt-replete individuals suggests that dopamine rather than 5-hydroxytryptamine was preferentially produced when equimolar amounts of their precursors were provided and that the natriuretic effect of dopamine, generated intrarenally from gludopa, was greater than the sodium retaining action of 5-hydroxytryptamine derived from γ-l-glutamyl-5-hydroxy-l-tryptophan. Comparison of the urinary metabolite data after the separate and concomitant infusion of the two glutamyl compounds provided no evidence of competitive inhibition of synthesis of either amine.

Atrial peptide potentiates renal responses to volume expansion in conscious dogs

1989 ◽  
Vol 256 (1) ◽  
pp. R284-R289
Author(s):  
C. H. Metzler ◽  
D. J. Ramsay
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Physiological Dose ◽  
Peptide Secretion ◽  
Renal Responses ◽  
Dose Dependent

Experiments were performed to compare the renal responses to atrial peptide infusion in conscious dogs with normal and expanded extracellular fluid volumes to test the hypothesis that the renal responses to atrial peptide infusions are dependent on the prevailing fluid and electrolyte status in the animal. Atrial peptide-(99-126) was infused intravenously in doses of either 0, 5, 25, or 100 ng.kg-1.min-1 in conscious dogs prepared with chronic catheters in the femoral artery and vein and the urinary bladder. In dogs with normal extracellular fluid volume, atrial peptide caused small increases in urinary sodium excretion with the high physiological (25 ng.kg-1.min-1) and pharmacological (100 ng.kg-1.min-1) doses. Urine volume and potassium excretion were increased only at the highest pharmacological dose. In contrast, atrial peptide infusion in dogs that were volume expanded by infusion of hypertonic saline showed dramatic, dose-dependent increases in sodium excretion and urine flow with all doses tested. The low, physiological dose of atrial peptide (5 ng.kg-1.min-1) increased sodium excretion and urine flow rate in volume-expanded dogs more than the pharmacological dose in normal dogs (n = 4). These results demonstrate that the renal responses to atrial peptide infusion are potentiated in dogs that are volume expanded and suggest that under conditions where atrial peptide secretion would be enhanced, small changes in plasma atrial peptide concentration can have significant effects on renal function.

Plasma Renin, Urinary Sodium Excretion and Vascular Disease

1974 ◽  
Vol 48 (s2) ◽  
pp. 127s-129s
Author(s):  
A. E. Doyle ◽  
K. G. Chua ◽  
S. Duffy ◽  
W. J. Louis
Keyword(s):  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Vascular Disease ◽  
Sodium Excretion ◽  
Mild Hypertension ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Renin Activity

1. Urinary sodium excretion and plasma renin activity have been measured in a group of persons with untreated mild hypertension and in a control normotensive group. 2. Preliminary analyses of the data indicate that the daily sodium excretion was significantly higher in the hypertensive group but the plasma renin activity did not correlate significantly with the urinary excretion of sodium. 3. These findings suggest that sodium intake was significantly greater in a population with mild hypertension than in a comparable normotensive group.

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