Renal urate excretion at various plasma concentrations in the rat: a free-flow micropuncture study

1976 ◽  
Vol 231 (2) ◽  
pp. 387-392 ◽  
Author(s):  
D De Rougemont ◽  
M Henchoz ◽  
F Roch-Ramel
Keyword(s):  
Plasma Concentrations ◽  
Proximal Tubules ◽  
Free Flow ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Micropuncture Study ◽  
Plasma Urate ◽  
Pelvic Urine

Free-flow micropuncture experiments were performed in male Sprague-Dawley rats undergoing moderate mannitol diuresis and infused with urate-containing solutions. The resulting plasma urate concentrations ranged from 37.5 +/- 2.4 to 601.2 +/- 23.8 muM. With urate loading, the fraction of filtered urate excreted in pelvic urine increased from 0.32 +/- 0.02 to 0.92 +/- 0.05 mu M, but net secretion was not observed. At normal urate levels net reabsorption occurred along superficial proximal tubules, whereas net secretion could be demonstrated at the highest plasma urate levels. Net movements of urate did not appear to occur across the walls of the lower segments of nephrons.

scholarly journals Oral absorption and drug interaction kinetics of moxifloxacin in an animal model of weightlessness

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong Liang ◽  
Jing Ma ◽  
Bo Wei
Keyword(s):  
Oral Dose ◽  
Oral Absorption ◽  
Jugular Vein ◽  
Plasma Concentrations ◽  
Pharmacokinetic Data ◽  
Simulated Weightlessness ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Interaction Kinetics ◽  
Kinetics Of

AbstractTo investigate the effect of simulated weightlessness on the pharmacokinetics of orally administered moxifloxacin and the antacid Maalox or the antidiarrheal Pepto-Bismol using a tail-suspended (TS) rat model of microgravity. Fasted control and TS, jugular-vein-cannulated, male Sprague-Dawley rats received either a single 5 mg/kg intravenous dose or a single 10 mg/kg oral dose of moxifloxacin alone or with a 0.625 mL/kg oral dose of Maalox or a 1.43 mL/kg oral dose of Pepto-Bismol. Plasma concentrations of moxifloxacin were measured by HPLC. Pharmacokinetic data were analyzed using WinNonlin. Simulated weightlessness had no effect on moxifloxacin disposition after intravenous administration but significantly decreased the extent of moxifloxacin oral absorption. The coadministration of moxifloxacin with Maalox to either control or TS rats caused significant reductions in the rate and extent of moxifloxacin absorption. In contrast, the coadministration of moxifloxacin with Pepto-Bismol to TS rats had no significant effect on either the rate or the extent of moxifloxacin absorption. These interactions showed dose staggering when oral administrations of Pepto-Bismol and moxifloxacin were separated by 60 min in control rats but not in TS rats. Dose staggering was more apparent after the coadministration of Maalox and moxifloxacin in TS rats.

Sepsis induces changes in the expression and distribution of Toll-like receptor 4 in the rat kidney

2006 ◽  
Vol 290 (5) ◽  
pp. F1034-F1043 ◽  
Author(s):  
Tarek M. El-Achkar ◽  
Xiaoping Huang ◽  
Zoya Plotkin ◽  
Ruben M. Sandoval ◽  
Georges J. Rhodes ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Expression Patterns ◽  
Cecal Ligation ◽  
Proximal Tubules ◽  
Microbial Pathogens ◽  
Sprague Dawley ◽  
Renal Vasculature ◽  
Two Photon Microscopy ◽  
Sprague Dawley Rats ◽  
Cellular Signal

Toll-like receptors (TLRs) are now recognized as the major receptors for microbial pathogens on cells of the innate immune system. Recently, TLRs were also identified in many organs including the kidney. However, the cellular distribution and role of these renal TLRs remain largely unknown. In this paper, we investigated the expression of TLR4 in a cecal ligation and puncture (CLP) model of sepsis in Sprague-Dawley rats utilizing fluorescence microscopy. In sham animals, TLR4 was expressed predominantly in Tamm-Horsfall protein (THP)-positive tubules. In CLP animals, TLR4 expression increased markedly in all tubules (proximal and distal), glomeruli, and the renal vasculature. The staining showed a strong apical distribution in all tubules. A moderately less intense cellular signal colocalized partially with the Golgi apparatus. In addition, kidneys from septic rats showed increased expression of CD14 and THP. They each colocalized strongly with TLR4, albeit in different tubular segments. We also imaged the kidneys of live septic animals with two-photon microscopy after fluorescent lipopolysaccharide (LPS) injection. Within 10 min, LPS was seen at the brush border of some proximal tubules. Within 60 min, LPS was fully cytoplasmic in proximal tubules. Conversely, distal tubules showed no LPS uptake. We conclude that TLR4, CD14, and THP have specific renal cellular and tubular expression patterns that are markedly affected by sepsis. Systemic endotoxin can freely access the tubular and cellular sites where these proteins are present. Therefore, locally expressed TLRs and other interacting proteins could potentially modulate the renal response to systemic sepsis.

Daily rhythm of NaCl intake in rats fed low-Ca2+ diet: relation to plasma and urinary minerals and hormones

1996 ◽  
Vol 270 (3) ◽  
pp. R505-R517 ◽  
Author(s):  
M. G. Tordoff ◽  
A. Okiyama
Keyword(s):  
Dark Period ◽  
Plasma Concentrations ◽  
Salt Appetite ◽  
Sprague Dawley ◽  
Lower Plasma ◽  
Plasma Osmolarity ◽  
Dihydroxyvitamin D3 ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
Plasma Phosphorus

To assess daily rhythms of salt appetite, we measured spontaneous 300 mM NaCl intake of male Sprague-Dawley rats fed a diet containing 150 or 25 mmol Ca2+/kg. Both groups drank most NaCl at night, but, as the dark period progressed, intakes of controls remained constant or diminished, whereas intakes of rats fed low-Ca2+ diet increased. During the late dark period, when the difference in NaCl intake between the two dietary groups was greatest, rats fed a low-Ca2+ diet lost more corticosterone and sodium in urine, had lower plasma osmolarity, and had higher plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations than did controls. Over the 24-h cycle, rats fed the low-Ca2+ diet excreted less Ca2+ and more corticosterone in urine than did controls. They also had consistently lower plasma concentrations of Ca2+ and renin activity and consistently higher plasma phosphorus, arginine vasopressin, parathyroid hormone, thyroxine, calcitonin, and 1,25-dihydroxyvitamin D3. These findings support the hypothesis that salt appetite induced by dietary Ca2+ deficiency involves a subtle dysfunction of the ACTH-corticosterone axis, but they also raise several other possibilities.

Central nervous system histamine regulates peripheral sympathetic activity

1991 ◽  
Vol 260 (1) ◽  
pp. H218-H224 ◽  
Author(s):  
V. F. Akins ◽  
S. L. Bealer
Keyword(s):  
Hypertonic Saline ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Central Administration ◽  
Sprague Dawley ◽  
Irreversible Inhibitor ◽  
Brain Histamine ◽  
Sprague Dawley Rats ◽  
H1 Antagonist ◽  
Peripheral Sympathetic Activity

Brain histamine (HA) was depleted in conscious Sprague-Dawley rats by central administration of alpha-fluoromethyl-histidine (alpha-FMH), an irreversible inhibitor of the HA synthesizing enzyme. Isotonic or hypertonic saline was infused intravenously at 10 microliters.100 g-1.min-1 for 30 min and mean arterial pressure (MAP) and heart rate (HR) were monitored. In addition, plasma vasopressin (AVP) and norepinephrine (NE) were measured pre- and postinfusion. Animals pretreated with alpha-FMH showed a delayed and attenuated pressor response and bradycardia during hypertonic saline (HTS) infusion and a significant reduction in plasma NE levels (-29 +/- 8% below control values). However, plasma concentrations of AVP were similar in both groups. Central pretreatment with the H1-antagonist pyrilamine (PYR) also delayed the onset and significantly attenuated the pressor response to HTS infusion, and caused dose-related decreases in plasma NE concentrations (-34 +/- 8, -47 +/- 5, and -52 +/- 7% after 60, 100, and 600 nmol PYR, respectively). These data indicate a role for central HA in peripheral sympathetic activation but not as a mediator of AVP release to a peripheral hyperosmotic stimulus.

Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors

1993 ◽  
Vol 136 (2) ◽  
pp. 283-288 ◽  
Author(s):  
C. P. Smith ◽  
R. J. Balment
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Plasma Concentrations ◽  
Receptor Subtypes ◽  
Vasopressin Receptor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anaesthetized Rat

ABSTRACT The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague–Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1′-methylpropyl)-2-thiobarbiturate) and infused with 0·077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1, d-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [β-mercapto-β,β-cyclopenta-methylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptor subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, All or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis. Journal of Endocrinology (1993) 136, 283–288

scholarly journals Changes of Plasma FABP4, CRP, Leptin, and Chemerin Levels in relation to Different Dietary Patterns and Duodenal-Jejunal Omega Switch Surgery in Sprague–Dawley Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Dominika Stygar ◽  
Elżbieta Chełmecka ◽  
Tomasz Sawczyn ◽  
Bronisława Skrzep-Poloczek ◽  
Jakub Poloczek ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Control Diet ◽  
Plasma Concentrations ◽  
Sprague Dawley ◽  
Fatty Acid Binding ◽  
Diet Patterns ◽  
Reactive Protein ◽  
Intestinal Length ◽  
Sprague Dawley Rats ◽  
Obesogenic Diet

Background. Pathophysiological links between inflammation, obesity, and adipokines can be used for the treatment of metabolic dysregulation. Aims. To examine the influence of duodenal-jejunal omega switch surgery in combination with different diet patterns on plasma concentrations of fatty acid-binding protein 4 (FABP4), C-reactive protein (CRP), leptin, and chemerin. Methods. After 8 weeks on a high-fat diet (HF) or control diet (CD), rats underwent surgery. Duodenal-jejunal omega switch (DJOS) with an exclusion of one-third of intestinal length and SHAM surgery were performed. For the next 8 weeks, 50% of DJOS/SHAM animals were kept on the same diet as before (HF/DJOS/HF, HF/SHAM/HF, CD/DJOS/CD, and CD/SHAM/CD), and 50% had a changed diet (HF/DJOS/CD, HF/SHAM/CD, CD/DJOS/HF, and CD/SHAM/HF). FABP4, CRP, leptin, and chemerin were assessed using ELISA kits. Results. FABP4: significant differences between DJOS and SHAM were observed in animals maintained on CD/CD; CRP: varied between DJOS and SHAM groups maintained on HF/HF, CD/CD, and CD/HF; leptin and chemerin levels: DJOS lowered leptin and chemerin plasma levels versus SHAM, while HF/HF, CD/HF, and HF/CD significantly increased leptin and chemerin plasma levels when compared to CD/CD. Conclusions. The beneficial effect of DJOS surgery is stronger than proinflammatory conditions caused by an HF obesogenic diet.

Physiological Amounts of Angiotensinogen Increase Blood Pressure in Sprague Dawley Rats After I.V. Administration.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 694-694
Author(s):  
Christoph P R Klett ◽  
Joey P Granger
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Transit Time ◽  
Mean Arterial Blood Pressure ◽  
Time Lag ◽  
Plasma Concentrations ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Arterial Blood ◽  
Sprague Dawley Rats

P9 The synthesis and secretion of hepatic angiotensinogen is controlled by a complex pattern of physiologic and pathophysiologic mediators including glucocorticoids, estrogens, thyroid hormones, cytokines, glucagon,insulin, and prostaglandins. Since plasma concentrations of angiotensinogen are close to the Michaelis Menten constant, it was hypothesized that changes in angiotensinogen plasma concentrations have an influence on the formation rate of angiotensin I and angiotensin II and, therefore, on blood pressure. To further test this hypothesis we injected purified rat angiotensinogen i.v. in Sprague Dawley rats via the femoral vein. Mean arterial blood pressure was measured after arterial cathederization. Control animals had a mean arterial pressure of 131 ± 2 mm Hg before and after the injection of vehicle (saline). The injection of 0.8, 1,2, and 2.9 mg/kg angiotensinogen caused a dose dependend increase in mean arterial blood pressure of 8 ± 0.4, 19.3 ± 2.1, and 32 ± 2.4 mm Hg, respectively. In contrast, the injection of a purified rabbit anti-rat-angiotensinogen antibody 1.4 mg/kg resulted in a significant decrease in blood pressure (-52 ± 3.2 mmHg). In an attempt to analyze how fast and efficient angiotensinogen production can sense regulatory input and convert into adaptation of secretion rate we determined the transit time (time needed for translation and post-translational modifications) for angiotensinogen in a pulse chase experiment employing 35 [S]-methionine as label in freshly isolated hepatocytes. During the chase periode, after quantitative immunoprecipitation, we determined the transit time for angiotensinogen with 2.5 h which is consistent with the constitutive type of angiotensinogen secretion and the time lag found for plasma concentrations to respond to regulatory mediators. In summary we conclude that variations in angiotensinogen plasma concentrations can result in changes in blood pressure. In contrast to renin known as a tonic regulator for the generation of angiotensin I, angiotensinogen seems to be a factor rather important for long-term control of the basal activity of the renin angiotensin system.

Renal excretion of uric acid in the rat: a micropuncture and microperfusion study

1976 ◽  
Vol 230 (3) ◽  
pp. 768-776 ◽  
Author(s):  
F Roch-Ramel ◽  
F Diezi-Chomety ◽  
D De Rougemont ◽  
M Tellier ◽  
J Widmer ◽  
...  
Keyword(s):  
Uric Acid ◽  
Renal Excretion ◽  
Proximal Tubules ◽  
Free Flow ◽  
Collecting Ducts ◽  
Order Of Magnitude ◽  
Plasma Urate ◽  
Distal Tubules

Free-flow micropuncture experiments were done in rats of three strains infused with small amounts of urate [plasma urate (P urate) = 95 +/- 8 muM]. Urate concentrations in tubular fluid were measured by an accurate chemical fluorometric ultramicromethod. In fluid from surface glomeruli, the glomerular fluid-to-plasma urate ratio [GF/P) urate] was 0.99 +/- 0.03 (n=11), i.e., lower than expected for total ultrafiltrability of plasma urate. Along proximal convolutions, net reabsorption of 55% of filtered urate was demonstrated. Small amounts of urate may have been reabsorbed between late proximal and early distal sites. Net transepithelial movements of urate did not occur in distal tubules or collecting ducts. In microperfusion experiments on proximal tubules, both a reabsorptive flow of urate (loss of perfused [2-14C]urate) and a secretory flow (entrance of cold urate into perfusate) of the same order of magnitude were demonstrated. Neither flow was influenced by simultaneous water movements. Microperfusion of Henle's loops indicated a significant but very small net reabsorption.

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