scholarly journals ANALYSIS OF INFLUENCE OF RUTIN AND GRAVITY ACTION ON THE RENAL EXCRETORY FUNCTION

2016 ◽  
Vol 1 (4) ◽  
pp. 47-50
Author(s):  
E N Zaitceva ◽  
A V Dubishchev ◽  
V A Kurkin
Keyword(s):  
Tubular Reabsorption ◽  
Diuretic Activity ◽  
Sodium Potassium ◽  
Water Load ◽  
Excretory Function ◽  
Series Of Experiments ◽  
Complex Influence ◽  
Renal Excretory Function ◽  
Tubular Component ◽  
Stimulation Of

Aim - to analyze the effect of rutin on the renal excretory function in the conditions of normogravity and hypergravity. Materials and methods. 9 series of experiments were conducted, including 4 series with the use of a centrifuge of ultra-short radius. The effect of rutin in the dose of 10 mg/kg on the renal excretory function was studied in normal conditions and in combination with the gravity action 3g. All the animals received 3% water load intragastrically and were placed into exchange cages for 24 hours. We obtained urine samples and determined the amount and the concentration of sodium, potassium and creatinine. Results. It was found that under normal conditions rutin, administered intragastrically in a dose of 10 mg/kg, promotes significant increase in diuresis and saluresis solely due to the inhibition of tubular reabsorption. Rutin in a dose of 10 mg/kg in combination with the gravity action enhances its original diuretic activity by complex influence on tubular and glomerular kidney structures. Rutin alone and rutin in combination with hypergravity stimulates the excretory function of the kidneys similarly to hydrochlorothiazide, but has a shorter latent period. Conclusion. The use of rutin combined with the gravity action contributes to the stimulation of the renal excretory function not only due to the tubular component, but also due to the glomerular one.

scholarly journals REGULATION OF THE EXCRETORY FUNCTION OF THE KIDNEYS BY MEANS OF ADENOSINERGICAL AGENTS

2018 ◽  
Vol 3 (3) ◽  
pp. 61-63
Author(s):  
EN N Zaitceva ◽  
AV V Dubishchev ◽  
AA A Bazitova
Keyword(s):  
Adenosine Receptors ◽  
Chloride Solution ◽  
Volume Concentration ◽  
Tubular Reabsorption ◽  
Sodium Potassium ◽  
Water Load ◽  
Excretory Function ◽  
Receptor Blockers ◽  
Isotonic Sodium Chloride ◽  
Dual Mechanism

Aim - study of the effect of agonist and antagonists of adenosine receptors on the excretory function of the kidneys. Materials and methods. The experiments were carried out on white outbread rats. Experimental animals were injected subcutaneously with a pharmacological agent (natrii adenosinetriphosphate, natrii coffeinum-benzoate, euphyllinum, pentoxifylline), control - a similar volume of isotonic sodium chloride solution. All animals received an intra-gastric water load of 3% ofbody weight. The animals were placed in the exchange cells. The portions of urine (4 h and 24 h) were collected. In each sample, the volume, concentration of sodium, potassium and creatinine was determined. Results. A diuretical dose for pentoxifylline 0.7 mg/kg was established. The drug in this dose stimulated the excretory function of the kidneys by increasing the glomerular filtration and inhibiting tubular reabsorption. Consequently, pentoxifylline has a dual mechanism of diuretic action - tubular (similar to the action of furosemide at a threshold dose of 1 mg/kg) and an additional glomerular component. Conclusion. The search for diuretics among adenosine receptor blockers is promising, especially in the line of new selective adenosinergic drugs.

Acute Effects of Acetazolamide (Diamox) on Plasma and Urinary Electrolytes of Dogs With Special Reference to Calcium

1957 ◽  
Vol 191 (2) ◽  
pp. 388-392 ◽  
Author(s):  
Smith Freeman ◽  
Anne B. Jacobsen
Keyword(s):  
Carbon Dioxide ◽  
Plasma Concentration ◽  
Chloride Concentration ◽  
Total Plasma ◽  
Acute Effects ◽  
Plasma Phosphate ◽  
Sodium Potassium ◽  
Excretory Function ◽  
Acute Increase ◽  
Renal Excretory Function

Administration of Diamox by ingestion or injection to adult fasting female dogs consistently produced an acute increase of approximately 1 mg % in the plasma concentration of calcium. At the same time there was an increase in the plasma phosphate and chloride concentration and a decrease in total plasma content of carbon dioxide of Diamox-infused dogs. Diamox did not affect the plasma concentration of calcium, chloride or bicarbonate if renal excretory function was abolished prior to its administration. Infusion of Diamox produced a prompt rise in the urinary excretion of sodium, potassium, calcium, phosphate, citrate, chloride and water in fasting female dogs. The effect of Diamox on the fasting concentration of calcium rendered unsatisfactory the interpretation of data concerned with a study of its effect on the disappearance of injected calcium. However, intravenous injection of small amounts of sodium carbonate was found to produce a definite delay in the rate of disappearance of injected calcium.

SODIUM EXCRETION IN THE ADRENALECTOMIZED RAT AFTER INTRAVENOUS SALINE INFUSION

1960 ◽  
Vol 20 (2) ◽  
pp. 112-122 ◽  
Author(s):  
C. J. EDMONDS
Keyword(s):  
Sodium Excretion ◽  
Tubular Reabsorption ◽  
Similar Extent ◽  
Sodium Potassium ◽  
Water Load ◽  
Initial Rise ◽  
Intravenous Saline ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Adrenalectomized Rats

SUMMARY The excretion of sodium, potassium and water, and the changes of glomerular filtration rate (g.f.r.) in response to intravenous infusions of hypertonic saline have been studied in normal and adrenalectomized rats. The increase in sodium excretion in response to infusion was considerably depressed after adrenalectomy. It was not restored to normal by cortisone or cortisol administration, although the adrenalectomized rats treated with these steroids were able to excrete water after a water load as rapidly as normal rats. Potassium excretion was increased to a similar extent by the infusions in both normal and adrenalectomized rats. g.f.r. rose in both groups during the infusion but the rise was depressed by adrenalectomy. In both normal and adrenalectomized rats treated with cortisone, g.f.r. remained elevated throughout the infusion, but the initial rise was less rapid in the latter than in the normal animals. In adrenalectomized rats maintained on 1% saline only, the rise of g.f.r. was not sustained and by the 4th hr of infusion had fallen to the pre-infusion level. When i.v. cortisol was given immediately before the infusion, the initial rise of g.f.r. was restored to normal. Comparison of the changes of g.f.r. with those of sodium excretion suggested that impairment of sodium excretion during the infusions was due, in part at least, to a change in renal tubular reabsorption of sodium following adrenalectomy.

Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2795-2800 ◽  
Author(s):  
R. Behm ◽  
H. Mewes ◽  
W. H. DeMuinck Keizer ◽  
T. Unger ◽  
R. Rettig
Keyword(s):  
Carotid Body ◽  
Normobaric Hypoxia ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Excretory Function ◽  
Arterial Blood ◽  
Peripheral Arterial ◽  
Renal Responses ◽  
Arterial Po2 ◽  
Sodium And Potassium

The contribution of peripheral arterial chemoreceptors to cardiovascular and renal responses to acute hypocapnic hypoxia is currently not well understood. We compared the effects of normobaric hypoxia on mean arterial blood pressure (MABP), heart rate, glomerular filtration rate (GFR), renal blood flow (RBF), and renal volume and electrolyte excretion in conscious unilaterally nephrectomized carotid body-denervated (n = 10) and sham-operated (n = 10) control rats. Thirty minutes of normobaric hypoxia (12.5% O2) resulted in significant reductions in arterial PO2 and PCO2 as well as decreases in MABP, GFR, RBF, and renal sodium, potassium, and water excretion. These effects occurred more rapidly and/or were significantly more pronounced in carotid body-denervated than in sham-operated rats. These data indicate that moderate acute hypocapnic hypoxia has profound effects on systemic and renal hemodynamics as well as on renal excretory function in conscious rats. We conclude that stimulation of the peripheral arterial chemoreceptors can partially offset the hypoxia-induced decreases in MABP, RBF, GFR, urine flow, and urinary sodium and potassium excretion, thereby helping to maintain cardiovascular as well as fluid and electrolyte homeostasis.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

Abstract 067: Mechanism of Action of 8-Aminoguanine on Renal Excretory Function

Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Edwin K Jackson ◽  
Zaichuan Mi ◽  
Thomas R Kleyman ◽  
Dongmei Cheng
Keyword(s):  
Mechanism Of Action ◽  
Excretory Function ◽  
Renal Excretory Function

Stimulation of avian renal phosphate secretion by parathyroid hormone

1981 ◽  
Vol 241 (3) ◽  
pp. F263-F272 ◽  
Author(s):  
R. F. Wideman ◽  
E. J. Braun
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Phosphate ◽  
Domestic Fowl ◽  
Inorganic Phosphate ◽  
Minor Component ◽  
Sodium Potassium ◽  
Tubule Lumen ◽  
Tubular Transport ◽  
A Minor ◽  
Stimulation Of

Phosphate buffers (ammonium, sodium, potassium, and calcium phosphate, pH 5.5, 7.2, 8.5) and 32P were infused unilaterally into the renal portal systems of intact, parathyroidectomized (PTX), and parathyroid hormone-infused (PTH) domestic fowl to study the secretory flux for inorganic phosphate (Pi). Urine samples were collected simultaneously from both kidneys, with the uninfused kidney serving as a control for the portal-perfused kidney (modified Sperber technique). No consistent unilateral excess of Pi or 32P excretion occurred for any of the experimental groups. For intact birds, fractional 32P excretion by both kidneys (FE32p) was identical to fractional Pi excretion (FEpi) (determined by chemical analysis) and reflected net reabsorption (0.64). However, during PTH infusion, FE32p was 0.82 (net reabsorption) while FEPi was 1.21 (net secretion). These results indicate that a) the peritubular-to-lumen flux for Pi and 32P is a minor component of net tubular transport, regardless of the parathyroid status, counterion availability, or peritubular Pi concentration; b) plasma Pi and 32P enter the tubule lumen predominantly by filtration; c) PTH stimulates tubular Pi secretion; and d) the secreted Pi is derived from an organic or inorganic pool that does not readily equilibrate with infused 32P (or presumably peritubular Pi).

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