Role of prostaglandins in the natriuresis of head-out water immersion in humans

1991 ◽  
Vol 80 (5) ◽  
pp. 481-488 ◽  
Author(s):  
Ton J. Rabelink ◽  
Hein A. Koomans ◽  
Evert J. Dorhout Mees
Keyword(s):  
Urinary Excretion ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Water Immersion ◽  
Chronic Administration ◽  
Relative Increase ◽  
Similar Degree ◽  
Acute Administration ◽  
Diluting Segment ◽  
Natriuretic Effect

1. Prostaglandins may play a role in the natriuresis seen after acute circulatory challenges. To assess this role in head-out water immersion, we compared, in clearance studies, the effects of acute (24 h) and chronic (7 days) administration of indomethacin, an inhibitor of prostaglandin synthesis, on the renal response to head-out water immersion in six healthy subjects on a 200 mmol of sodium/day diet and on a 40 mmol of sodium/day diet. 2. Indomethacin caused a similar degree of sodium retention on each of these two diets. 3. During the 40 mmol of sodium/day diet, acute administration of indomethacin decreased sodium excretion before, as well as during, head-out water immersion; however, the relative increase caused by head-out water immersion was normal. After chronic administration of indomethacin, both baseline sodium excretion and the natriuresis induced by head-out water immersion were similar to those in control studies. 4. During the 200 mmol of sodium/day diet, indomethacin had no effect on baseline sodium excretion, nor on the natriuretic effect of head-out water immersion. 5. Head-out water immersion decreased tubular lithium reabsorption and increased diluting segment delivery. Despite opposite effects of indomethacin on these parameters, indomethacin did not prevent the tubular effects of head-out water immersion on either diet. However, indomethacin did prevent the marked increase in estimated renal plasma flow and the fall in filtration fraction that were observed during head-out water immersion in the absence of indomethacin (control). 6. Head-out water immersion was not associated with an increase in urinary excretion of prostaglandins. Indomethacin lowered baseline urinary excretion of prostaglandins, which did not change further during head-out water immersion. 7. We therefore conclude that renal prostaglandins are not essential for a normal natriuretic response to head-out water immersion, although they may mediate the vasodilatation induced by head-out water immersion.

Role of ANP in natriuresis of head-out immersion in humans

1989 ◽  
Vol 257 (3) ◽  
pp. F375-F382 ◽  
Author(s):  
T. J. Rabelink ◽  
H. A. Koomans ◽  
P. Boer ◽  
C. A. Gaillard ◽  
E. J. Dorhout Mees
Keyword(s):  
Renal Plasma Flow ◽  
Water Immersion ◽  
Free Water ◽  
Urine Osmolality ◽  
Sodium Absorption ◽  
Free Water Clearance ◽  
Target Segment ◽  
Small Rise ◽  
Natriuretic Effect

Atrial natriuretic peptide (ANP) may play a role in the natriuresis after acute circulatory challenges. To assess this role in head-out water immersion (HOI), we compared in clearance studies the effect of 3 h HOI with an equally natriuretic 3-h infusion of ANP [0.01 microgram.kg-1.min-1 human ANP-(99-126)] in seven healthy individuals taking a 100 mmol sodium diet. The studies were repeated after treatment with enalapril (20 mg twice daily), which in previous studies inhibited the natriuresis after ANP. HOI caused a natriuresis equal to that of ANP infusion despite an about five times smaller rise in plasma ANP. HOI increased and ANP decreased estimated renal plasma flow (ERPF). HOI increased maximal free water clearance and decreased fractional lithium reabsorption. ANP did not affect these variables but raised minimal urine osmolality. Enalapril enhanced the fall in ERPF caused by ANP and abolished its natriuretic effect; enalapril did not impair either the natriuresis after HOI or the increase in ERPF and the fall in lithium reabsorption. These data indicate that the low dosage of ANP causes natriuresis by reducing sodium absorption in a distal nephron target segment; enalapril impairs this effect, perhaps by enhancing ANP-induced vasoconstriction, which decreases delivery to this target segment. HOI, by increasing sodium delivery to this segment, is natriuretic despite only a small rise in plasma ANP. Enalapril does not impair these effects. Although a rise in plasma ANP may be one factor in the natriuresis of HOI, the present data speak against an exclusive role. Other factors determine the magnitude of the natriuretic response.

Control of renal hemodynamics after protein feeding: role of calcium channels

1992 ◽  
Vol 263 (6) ◽  
pp. F1044-F1050 ◽  
Author(s):  
L. L. Woods ◽  
B. E. Smith ◽  
D. R. De Young
Keyword(s):  
Calcium Channels ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Amino Nitrogen ◽  
Renal Hemodynamics ◽  
Similar Degree ◽  
Meat Meal ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Protein Feeding

This study was designed to test the hypothesis that the changes in renal hemodynamics that occur after a high-protein meal involve voltage-dependent calcium channels. In chronically instrumented female dogs, a 10-g/kg meal of raw beef caused plasma alpha-amino nitrogen levels to increase from 3.9 +/- 0.2 to 6.7 +/- 0.5 mg/dl after 90 min, and glomerular filtration rate (GFR) rose from 59 +/- 6 to 85 +/- 7 ml/min, effective renal plasma flow (ERPF) rose from 130 +/- 22 to 213 +/- 36 ml/min, and sodium excretion rose from 21 +/- 4 to 84 +/- 20 mu eq/min. On another day the dogs were pretreated with verapamil (0.075 mg/kg + 0.005 mg.kg-1.min-1 iv), which did not change arterial pressure significantly but increased GFR by 25 +/- 7% and ERPF by 23 +/- 5%. After a subsequent meat meal, plasma alpha-amino nitrogen increased from 4.0 +/- 0.3 to 6.6 +/- 0.1 mg/dl but GFR, ERPF, and sodium excretion did not change significantly. On the other hand, pretreatment with dopamine, which caused a similar degree of vasodilation to that caused by verapamil, did not prevent the response to a subsequent meat meal. Thus verapamil specifically prevented the normal increases in renal hemodynamics after protein feeding, suggesting that protein-stimulated renal vasodilation requires intact voltage-dependent calcium channels.

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 natriuretic peptide in preeclampsia: metabolic clearance, sodium excretion and renal hemodynamics

1997 ◽  
Vol 273 (3) ◽  
pp. F483-F487 ◽  
Author(s):  
D. W. Irons ◽  
P. H. Baylis ◽  
T. J. Butler ◽  
J. M. Davison
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Metabolic Clearance ◽  
Significant Difference ◽  
Basal Plasma ◽  
Natriuretic Effect ◽  
Atrial Natriuretic

To further elucidate the role of atrial natriuretic peptide (ANP) in preeclampsia, its metabolic clearance (MCRANP) was determined concomitantly with its effects on sodium excretion (UNa), glomerular filtration rate (GFR), and effective renal plasma flow (ERPF). Ten untreated preeclamptic primigravidae (PET) were studied at 29-37 wk gestation and again 4 mo postpartum (PP). Basal plasma concentration of ANP was significantly increased in PET compared with PP (14.8 +/- 1.9 vs. 4.1 +/- 0.5 pmol/l, respectively; P < 0.0001). MCRANP in PET and PP was 5.0 +/- 0.8 and 4.9 +/- 0.5 l/min [not significant (NS)], respectively. In PET, infusion of ANP produced (basal vs. ANP) a natriuresis (UNa 0.14 +/- 0.02 vs. 0.28 +/- 0.04 mmol/min, P < 0.001) and an increase in GFR (97 +/- 7 vs. 106 +/- 8 ml/min, P < 0.05), with ERPF unchanged (609 +/- 24 vs. 634 +/- 29 ml/min, NS). In PP, ANP infusion also produced a natriuresis (UNa 0.20 +/- 0.02 vs. 0.25 +/- 0.02 mmol/min, P = 0.01), no significant change in GFR (109 +/- 7 vs. 102 +/- 4 ml/min), and a significant reduction in ERPF (514 +/- 22 vs. 409 +/- 18 ml/min, P < 0.0001). Analysis of variance demonstrated a greater natriuretic effect of ANP in PET compared with PP (P < 0.05), similarly a significant difference in the effect of ANP on ERPF (P < 0.01) and GFR (P < 0.05) was seen but not on filtration fraction (P = 0.35).

scholarly journals Endothelin induces diuresis and natriuresis in the rat by acting on proximal tubular cells through a mechanism mediated by lipoxygenase products.

1991 ◽  
Vol 2 (1) ◽  
pp. 57-69
Author(s):  
N Perico ◽  
R P Cornejo ◽  
A Benigni ◽  
B Malanchini ◽  
J R Ladny ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Atrial Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Lipoxygenase Products ◽  
Natriuretic Effect

Besides being a potent renal vasoconstrictor, endothelin causes diuresis and natriuresis. At which site along the nephron and how endothelin alters water and sodium handling in the tubule remain to be clarified. It was found that endothelin (75 pmol) given as an i.v. infusion in vivo to rats caused diuresis and urinary sodium excretion to double but did not affect glomerular filtration rate and renal plasma flow. On raising the dose of endothelin to 150 pmol, a further increase in diuresis and natriuresis was found, whereas glomerular filtration rate fell 33% and renal plasma flow fell 36%; 300 pmol of endothelin reduced glomerular filtration rate by 73% and renal plasma flow by 77% but did not significantly affect diuresis and absolute sodium excretion. It did, however, increase fractional sodium excretion eightfold. Lithium clearance studies of changes in tubular handling of water and sodium indicated that infusion of 150 pmol of endothelin to rats caused a reduction in absolute (pre, 84.7 +/- 5.9; post, 47.9 +/- 6.1 microEq/min/100 g) and fractional (pre, 85.7 +/- 3.0; post, 64.7 +/- 6.4%) proximal reabsorption of sodium. Endothelin infusion (150 pmol) was not associated with any significant change in plasma atrial natriuretic peptide levels, which on average remained comparable to those in rats given the vehicle alone (49.7 +/- 8.4 versus 46.3 +/- 5.6 pg/mL). In the isolated perfused rat kidney preparation, exposure to 150 pmol of endothelin significantly increased fractional sodium excretion over preinjection values (pre, 2.2 +/- 0.2; post, 7.3 +/- 1.0%) despite a marked decrease in glomerular filtration rate and renal perfusate flow. Additional in vivo experiments showed that oral administration of the specific 5-lipoxygenase inhibitor L-651,392 to rats prevented the increase in urine flow rate (pre, 5.7 +/- 0.1; post, 6.6 +/- 0.8 microL/min), and in absolute (pre, 0.33 +/- 0.04; post, 0.37 +/- 0.05 microEq/min) and fractional (pre, 0.10 +/- 0.02; post, 0.11 +/- 0.03%) sodium excretion caused by bolus i.v. infusion of endothelin (150 pmol). Similarly, a specific leukotriene C4/D4 receptor antagonist, L-649,923, also prevented the diuretic and natriuretic effect of 150 pmol of endothelin i.v. infusion. These findings show that (1) endothelin has a diuretic and natriuretic effect that is independent of its action on renal hemodynamics; (2) this effect depends on a direct action on the proximal tubules; (3) atrial natriuretic peptide does not appear to be involved in this effect; and (4) the diuretic and natriuretic responses to endothelin are mediated by 5-lipoxygenase products.

Antioxidant Supplementation and Adaptive Response to Training: A Systematic Review

2019 ◽  
Vol 25 (16) ◽  
pp. 1889-1912 ◽  
Author(s):  
Rosario Pastor ◽  
Josep A. Tur
Keyword(s):  
Antioxidant Enzymes ◽  
Cellular Response ◽  
Recovery Period ◽  
Chronic Administration ◽  
Antioxidant Response ◽  
Redox Status ◽  
Exercise Session ◽  
Acute Administration ◽  
Antioxidant Supplementation ◽  
Antioxidant Supplements

Background: Antioxidant supplementation has become a common practice among athletes to theoretically achieve a reduction in oxidative stress, promote recovery and improve performance. Objective: To assess the effect of antioxidant supplements on exercise. Methods: A systematic literature search was performed up to January 2019 in MEDLINE via EBSCO and Pubmed, and in Web of Sciences based on the following terms: “antioxidants” [Major] AND “exercise” AND “adaptation”; “antioxidant supplement” AND “(exercise or physical activity)” AND “(adaptation or adjustment)” [MesH]. Thirty-six articles were finally included. Results: Exhaustive exercise induces an antioxidant response in neutrophils through an increase in antioxidant enzymes, and antioxidant low-level supplementation does not block this adaptive cellular response. Supplementation with antioxidants appears to decrease oxidative damage blocking cell-signaling pathways associated with muscle hypertrophy. However, upregulation of endogenous antioxidant enzymes after resistance training is blocked by exogenous antioxidant supplementation. Supplementation with antioxidants does not affect the performance improvement induced by resistance exercise. The effects of antioxidant supplementation on physical performance and redox status may vary depending on baseline levels. Conclusion: The antioxidant response to exercise has two components: At the time of stress and adaptation through genetic modulation processes in front of persistent pro-oxidant situation. Acute administration of antioxidants immediately before or during an exercise session can have beneficial effects, such as a delay in the onset of fatigue and a reduction in the recovery period. Chronic administration of antioxidant supplements may impair exercise adaptations, and is only beneficial in subjects with low basal levels of antioxidants.

scholarly journals Exendin-4 increases blood glucose levels acutely in rats by activation of the sympathetic nervous system

2010 ◽  
Vol 298 (5) ◽  
pp. E1088-E1096 ◽  
Author(s):  
Diego Pérez-Tilve ◽  
Lucas González-Matías ◽  
Benedikt A. Aulinger ◽  
Mayte Alvarez-Crespo ◽  
Manuel Gil-Lozano ◽  
...  
Keyword(s):  
Nervous System ◽  
Blood Glucose ◽  
Sympathetic Nervous System ◽  
Mammalian Species ◽  
Chronic Administration ◽  
Acute Administration ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Sympathetic Nervous ◽  
High Doses

Exendin-4 (Ex-4), an agonist of the glucagon-like peptide-1 receptor (GLP-1R), shares many of the actions of GLP-1 on pancreatic islets, the central nervous system (CNS), and the gastrointestinal tract that mediates glucose homeostasis and food intake. Because Ex-4 has a much longer plasma half-life than GLP-1, it is an effective drug for reducing blood glucose levels in patients with type 2 diabetes mellitus (T2DM). Here, we report that acute administration of Ex-4, in relatively high doses, into either the peripheral circulation or the CNS, paradoxically increased blood glucose levels in rats. This effect was independent of the insulinotropic and hypothalamic-pituitary-adrenal activating actions of Ex-4 and could be blocked by a GLP-1R antagonist. Comparable doses of GLP-1 did not induce hyperglycemia, even when protected from rapid metabolism by a dipeptidyl peptidase IV inhibitor. Acute hyperglycemia induced by Ex-4 was blocked by hexamethonium, guanethidine, and adrenal medullectomy, indicating that this effect was mediated by sympathetic nervous system (SNS) activation. The potency of Ex-4 to elevate blood glucose waned with chronic administration such that after 6 days the familiar actions of Ex-4 to improve glucose tolerance were evident. These findings indicate that, in rats, high doses of Ex-4 activate a SNS response that can overcome the expected benefits of this peptide on glucose metabolism and actually raise blood glucose. These results have important implications for the design and interpretation of studies using Ex-4 in rats. Moreover, since there are many similarities in the response of the GLP-1R system across mammalian species, it is important to consider whether there is acute activation of the SNS by Ex-4 in humans.

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.

Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

1987 ◽  
Vol 252 (1) ◽  
pp. F91-F98
Author(s):  
R. D. Manning
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Renal Hemodynamics ◽  
Fluid Volume ◽  
Urinary Sodium ◽  
Plasma Aldosterone Concentration

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.

scholarly journals Chronic administration of furosemide augments renal weight and glomerular capillary pressure in normal rats

1998 ◽  
Vol 275 (2) ◽  
pp. F230-F234 ◽  
Author(s):  
Pascale H. Lane ◽  
Larry D. Tyler ◽  
Paul G. Schmitz
Keyword(s):  
Renal Injury ◽  
Wistar Rats ◽  
Chronic Administration ◽  
Relative Increase ◽  
Hydraulic Pressure ◽  
Ang Ii ◽  
Filtration Fraction ◽  
Renal Growth ◽  
Glomerular Capillary ◽  
Arteriolar Resistance

Angiotensin II (ANG II) is believed to promote progressive renal injury via augmented glomerular capillary hydraulic pressure (PGC). Acute volume reduction secondary to diuretic administration increases circulating ANG II and augments PGC, yet the hemodynamic effects of sustained diuretic administration are unknown. Therefore, glomerular micropuncture studies were performed in male Munich-Wistar rats after 6–8 wk of treatment with daily furosemide (F, 40 mg/day), furosemide plus the AT1 receptor antagonist, losartan (F + L, 5 mg/day), or no therapy (C, control). Renal weight was increased in F rats (1.23 ± 0.7 g) vs. C (1.00 ± 0.06 g) or F + L (0.97 ± 0.01 g). In addition, PGC was elevated in F animals (52.1 ± 1.5 mmHg) vs. C (43.7 ± 1.5) or F + L-treated rats (41.3 ± 1.7). F-treated rats were also characterized by a relative increase in efferent arteriolar resistance and filtration fraction. The latter was markedly attenuated in F + L-treated animals. Collectively, these findings are consistent with an ANG II-mediated alteration in intrarenal hemodynamics. In contrast to acute volume manipulations, however, chronic furosemide augmented renal growth, whereas losartan administration completely arrested this phenomenon. Further studies are warranted to determine whether the hemodynamic and growth adaptations elicited by chronic F administration induce or accelerate renal injury.

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