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Biomedical subjects

G Kövér

Publications and source records attributed to G Kövér.

At least 19 recordsLinked to original sources
PubMed1998

In vivo assessment of breast muscle, abdominal fat and total fat volume in meat-type chickens by magnetic resonance imaging.

Measurements were performed on commercial broiler chickens by magnetic resonance imaging (MRI) tomography. A total of 72 chickens were scanned at the age of 6, 7, 8, 10, 16 and 20 weeks. MRI scans based on spin echo sequence were taken in the three orthogonal planes. The volume of the pectoral muscles increased from 259 cm3 to 1035 cm3 in males and from 250 cm3 to 875 cm3 in females between 6 and 20 weeks of age. Abdominal fat volume increased from 18.9 cm3 to 153.2 cm3 in males and from 19.3 cm3 to 267.0 cm3 in females between 7 and 20 weeks of age. Total body fat volume increased from 129 cm3 to 557 cm3 in males and from 171 cm3 to 1321 cm3 in females between 6 and 20 weeks of age. The correlation coefficients between the total volume of fat pixels and the amount of abdominal fat determined in the coronal plane by MRI were 0.85 and 0.95 in the male and female sex, respectively. Changes found in the pectoral muscles (mm. pectorales) as well as in total and abdominal fat volume were in close agreement with dissection data obtained at the slaughterhouse and with laboratory data based on the measurement of total body chemical composition in both sexes. This MRI method can be a good complement to computed tomography (CT) scanning in the transversal plane.

Adipocytes↗
PubMed1997

[Principles of functional MRI imaging and its possibilities in the study of cerebral cortex activation].

While MR imaging of anatomic structures has long been widely appreciated, the emergence of functional magnetic resonance imaging (FMRI) methods for localising brain activity has emerged in the beginning of the 90s. This new MRI technique produces images of activated brain regions by detecting the indirect effects of neural activity on local blood volume, flow and oxygen saturation, and it is a promising new tool for further understanding of the relationships among brain structure, function and pathology. The information revealed by FMRI is partially overlapping with PET and SPECT, but it is non-invasive and has a better spatial and temporal resolution. The authors briefly summarise the concept and basics of FMRI and demonstrate the first successful FMRI examination performed in Hungary. The potential role of FMRI in the clinical practice is presented.

Animals↗
PubMed1995

Conjugate effects of saralasin and indomethacin on kidney function in anesthetized dog.

The intravenous administration of the cyclooxigenase blocking indomethacin results in a very rapid and sharp decrease of renal blood flow (RBF) and in a decrease of water and sodium excretion in anesthetized dogs. The result is very similar to that of the angiotensin II infusion. The present study was undertaken to examine in anesthetized dogs, how the angiotensin II receptor antagonist saralasin can influence the kidney function and the renal effects of the intravenously administered indomethacin. 0.2 micrograms/kg/min saralasin infused directly into the left renal artery induced a slight drop in the arterial blood pressure, and a slight but significant decrease in the renal vascular resistance without affecting other renal parameters. The intrarenal infusion of saralasin, when it preceded the administration of indomethacin, almost completely abolished the renal hemodynamic effects of indomethacin and decreased its effect on the renal water and sodium excretion. It seems therefore probable that in anesthetized dogs the renin-angiotensin system may play a role in the development of the renal effects of indomethacin.

Anesthesia↗
PubMed1995

Effect of volume expansion induced by Ringer's solution or plasma on the natriuretic response of the kidney.

Studies were carried out in anaesthetized dogs, to determine the effects of volume expansion induced by Ringer's solution, plasma taken from non-hydrated or previously volume expanded animals on the natriuretic response of the kidney. When the animals were infused with Ringer's solution (0.25 ml/kg/min iv.) water and sodium excretion increased gradually reaching a peak value at about 70 min. after starting the infusion (3.01 +/- 0.21 ml/min and 329 +/- 23.9 mmol/min, respectively). Infusing the dogs with plasma taken from non-hydrated animals (0.25 ml/kg/min iv.) water and sodium excretion showed a small increase in the first 15 min, but afterwards there was hardly any change in them, and water and sodium excretions were significantly less in the remaining part of the experiment than in with Ringer's solution expanded animals. (Peak values 1.44 +/- 0.53 ml/min and 193 +/- 85.3 mmol/min.) In animals infused with plasma taken from previously hydrated dogs (0.25 ml/kg/min iv.) water and sodium excretion were already after the first 15 min significantly higher than in the two other groups, they increased further in the following 15 to 30 minutes and remained elevated during the time of the study. (Peak values for water and sodium excretion being 3.30 +/- 0.58 ml/min and 344 +/- 73.5 mmol/l.) Blood pressure, CPAH and glomerular filtration rate were the same and did not change in either of the experimental series. We concluded, that besides the physical forces playing certainly a role mainly in the Ringer's solution hydrated dogs, some humoral natriuretic factor liberated in the volume expanded animals plays also a role in the diuretic-natriuretic response. This humoral factor can be released from the atria or other organs, but its production is not primarily regulated by intravasal volume/or pressure changes.

Animals↗
PubMed1994

The renal actions of adenosine.

This study examined the effects of adenosine on the renal function. In ten normal dogs intrarenal adenosine infusion (20 nmol/kg/min) increased the renal blood flow (RBF) from 521 +/- 20 ml/min to 582 +/- 23 ml/min. The extraction of PAH (EPAH) decreased from 0.85 +/- 0.02 to 0.79 +/- 0.02, the Einulin from 0.24 +/- 0.02 to 0.18 +/- 0.02. We conclude that the intrarenal infusion of adenosine modifies the intrarenal redistribution of the blood flow increasing the deep cortical and medullary blood flow. In these experiments the glomerular filtration (GFR) during adenosine infusion calculated from the extraction of the inulin (Einulin) multiplied by the renal plasma flow (RPF) decreased from 79.4 +/- 6.4 ml/min to 62.2 +/- 6.6 ml/min and calculated from the Ecreatinine x RPF from 80.3 +/- 6.3 ml/min to 59.3 +/- 4.9 ml/min. The EPAH x RPF did not change, it was 241 +/- 11 ml/min and 253 +/- 13 ml/min, respectively. While the urinary clearances (the clearance calculated by the classic clearance formula; urinary concentration of the substance multiplied by the urine volume and divided by the plasma concentration) in the control periods did not differ from the direct clearances (Cinulin = 73.3 +/- 3 ml/min, Ccreatinine = 75 +/- 4 ml/min and CPAH = 262 +/- 15 ml/min) during the adenosine infusion there are considerable differences: the Cinulin = 40 +/- 6 ml/min, the Ccreatine = 42 +/- 6 ml/min and the CPAH = 164 +/- 22 ml/min. The differences are mathematically significant (p < 0.01). During the postinfusion periods the urinary clearances did not differ from the direct clearances. These results show that during adenosine infusion there is a definitive loss of the clearance substances somewhere in the nephron between the glomeruli and the pyelon. These observations suggest that during adenosine infusion there is a back-diffusion of the clearance substances because the permeability of the tubuli changes in the medullary part. The rediffused substances will be retransported into the circulation by the renal lymph flow and that is why they do not appear in the renal venous blood. The rediffusion can explain that the intrarenal adenosine infusion decreases considerably the excretion of the sodium and water in the kidney when there is no or only a small reduction of the glomerular filtration rate.

Adenosine↗
PubMed1993

Effects of hypercalcemia on kidney function in anesthetized dogs.

The effects of acute hypercalcemia on renal function were evaluated in anesthetized mongrel dogs. Calcium concentration was increased by infusion of CaCl2 solution into the left renal artery at two different rates. At the lower rate of infusion (0.010 mM/kg/min) the plasma total calcium concentration in the left kidney increased from 2.5 mM/l to 3.76 mM/l and the arterial plasma total calcium concentration to 2.94 mM/l. Renal vascular resistance in the left kidney did not change in association with a small decrement in the renal blood flow (9.5%). The glomerular filtration rate decreased from 82.9 ml/min to 65.9 ml/min in association with a small decrease in the urine output. The calcium excretion increased slightly from 3.3 microM/min to 4.05 microM/min. When this amount of CaCl2 was infused into the left renal artery the parameters of the right intact kidney did not change. During the higher rate of infusion (0.020 mM/kg/min) in the left kidney the plasma total calcium concentration in the left kidney increased from 2.3 mM/l to 6.15 mM/l and in the arterial plasma to 3.4 mM/l. Renal vascular resistance increased considerably from 1.66 to 4.0 and the renal blood flow decreased from 482 ml/min to 311 ml/min. The glomerular filtration rate dropped from 78.7 ml/min to 43 ml/min with a significant decrease in the urine output. The calcium excretion increased from 4.35 microM/min to 7.5 microM/min. In the right kidney during the CaCl2 infusion the CPAH decreased from 304 ml/min to 239 ml/min showing that there was an increase in the vascular resistance in association with decrements in Cinulin from 85 ml/min to 67.2 ml/min. These data prove a direct, but not linear relationship between the total plasma calcium concentration and the renal vascular resistance. We suppose that the distal tubular calcium load participates in the distal tubular feedback regulation, when the calcium ion concentration in the tubular fluid at the macula densa increases. This increment elicits vasoconstriction in the afferent arteriole decreasing the filtered calcium load in the glomeruli.

Acute Disease↗
PubMed1991

Investigations on the circulation of anesthetized dogs.

In the present experiments arterial blood pressure, cardiac output, heart rate, oxygen consumption, AVO2 difference values and their changes were investigated in 64 anesthetized dogs in four periods for altogether 60 min. Blood flows of the renal, commune carotid and femoral arteries were measured in parallel and the changes were recorded throughout the 60 min of the experimental period. Urine was collected separately from both kidneys, in order to determine whether the measurement of the blood flow of the renal artery disturbed renal functions. Total peripheral vascular resistance and the vascular resistance of the territories of the commune carotid and femoral arteries were calculated from the parameters measured. In the present experiments the equation of the regression line between cardiac output and body weight was y = 0.102x + 0.9411. The equation of the regression line between cardiac output an body surface proved to be y = 2.996x + 0.653. The relationship between total oxygen consumption and body weight could be characterized by the y = 5.815x + 24.227 equation. Our data were in accordance with data of the Biology Data Book obtained in dogs anesthetized by pentobarbital. Our present data can be found but partially in the Biology Data Book, so the results obtained in the present study may serve as basis of future comparisons. In this work proper care was taken to maintain the same conditions and, thus ruling out possible artefacts. The experiments were carried out on mongrel dogs of different sexes; nevertheless, the animals were attempted to be kept under the same conditions for the 14 days preceding the experiments.

Anesthesia↗
PubMed1990

The effect of lidocain on the renal function.

The evidence supporting a role for direct neurogenic control of renal function was investigated in twenty anaesthetized dogs. Unilateral renal sympathectomy was induced by 0.5 mg/kg/min of lidocain infusion into the left renal artery and the kidney function changes were compared to those observed in the right non infused kidney. The renal parameters were similar in the kidneys during the control periods. 0.5 mg/kg/min of lidocain infusion into the left renal artery resulted in significant reductions of the RBF, GFR, urine and sodium excretion in the left kidney. The intrarenal lidocain infusion induced a small decrease of the arterial blood pressure but this can not explain the changes observed in the left kidney. The modifications of the right kidney function during lidocain infusion were significantly less than those observed in the left kidney. Comparing the measured RBF and the renal blood flow calculated by the CPAH in the left kidney during the lidocain infusion, we have found a marked difference, when the decrease of the calculated RBF was greater. We believe that effects of pharmacological denervation can be best explained by the intrarenal hemodinamically mediated changes. The sympathectomy produces a considerable vasoconstriction in the renal cortical vascular bed, subsequently it decreases the RBF, GFR renal sodium and water excretion. But the lidocain blocks the sympathetic nerves influencing the renal medullary vessels and the renal medullary blood flow increases. These observations are not consistent with the notion that renal nerves are at least partially responsible for the natriuresis accompanying salt loading.

Animals↗
PubMed1989

The effect of Ringer solution induced extracellular volume expansion on kidney function.

The present study quantitated the effects of extracellular volume expansion on sodium and water excretion in 118 anesthetized dogs. The animals received a priming injection of 10 ml kg-1 Ringer solution i.v. which was followed by a constant Ringer solution infusion at a rate of 0.25 ml.min-1.kg-1 until the end of the experiment. Fifteen minutes after the start of the constant infusion the renal parameters were examined in 11 subsequent 15 min periods (the total time was 3 hours). Volume expansion produced no significant change in arterial blood pressure, glomerular filtration rate (GFR), plasma sodium and potassium concentration or, haematocrit, but did reduce the CPAH from 284 ml.min-1 to 218 ml.min-1 (the data were calculated for 100 gram wet kidney weight). There were constant significant increases in the urinary excretion rate from 0.84 ml.min-1 to 4.06 ml.min-1 and the 39% of the infused water was excreted during the experiment. Volume expansion also caused a significant increase in sodium excretion during the three first periods from 120 mumol.min-1 to 329 mumol.min-1 followed by a small but significant decrease. The sodium excretion at the end of the experiment was 221 mumol.min-1 and the 23% of the infused sodium was excreted in the course of the experiment. The increase of the water excretion during the volume expansion was associated with fall of the urine osmolality and the urine because hypoosmotic as compared to the plasma. We have provided evidence that vasopressin was not involved in the control of water excretion in our experiments. It is concluded that neither filtered sodium nor decreased aldosterone secretion can account for the increase in sodium excretion that occurs after Ringer solution loading in the dog. It has been proposed that a decrease in plasma protein concentration may decrease passive sodium reabsorption due to oncotic forces in the proximal tubule. The Ringer solution diuresis elicits a rise in medullary blood flow, thereby causing a washout of medullary sodium. This might dissipate the osmotic force for the back-diffusion of water from the collecting duct. Our studies indicate that the response of the diluting segments of the distal nephron to increased delivery of sodium depends upon the presence or absence of volume expansion. However the increase of the distal tubular loading activates the tubuloglomerular feedback which increases the proximal tubular reabsorption. Based on these assumptions our studies provide further evidence that the tubuloglomerular feedback regulates the blood pressure in the peritubular capillaries in the cortex around the proximal tubules.

Animals↗
PubMed1989

The effects of clonidine on the kidney function in the anesthetized dog.

Studies were performed to determine the mechanism by which the antihypertensive agent clonidine increased urine flow. The response of the kidney has been examined in four combinations. The parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution. In the control animals, volume expansion by 2% body weight, resulted in a slight increase in sodium excretion and urine flow. In 10 anesthetized dogs 1.0 microgram/kg/min of clonidine infused i.v. during 30 minutes (the total amount of clonidine infused was 30 micrograms/kg) decreased the arterial blood pressure from 136 +/- 13 mmHg to 127 +/- 12 mmHg and elevated urine flow from 2.95 +/- 1.65 ml/min to 4.34 +/- 1.77 ml/min while the urine osmolality diminished from 399 +/- 107 mosm/l to 265 +/- 90 mosm/l and the glomerular filtration remained constant. In 5 animals 0.1 microgram/kg/min of clonidine was infused into the left renal artery (this dose is corresponding to the renal fraction of the cardiac output) without any effects in the left kidney. 1.0 microgram/kg/min of clonidine infused directly into the left renal artery produced vasoconstriction in the ipsilateral kidney, decreased the glomerular filtration rate and the urine flow. By contrast in the right kidney the urine flow rose without hemodynamic changes, and the urine osmolality became hypoosmotic compared to the plasma. In ten dogs 1.0 microgram/kg/min of clonidine and 1 mU/kg/min of arginine-vasopressin were infused intravenously. The vasopressin infusion superimposed on the clonidine could not inhibit the increase of the urine excretion, and the fall of the urine osmolality. The results suggest that the clonidine increases the renal medullary blood flow possibly via a direct mechanism, decreases the sympathetic outflow to the kidney and via an indirect pathway, mediated by the renin-angiotensin system. The renal medullary flow increase produces a washout of the medullary osmotic gradient, and the water reabsorption diminishes.

Anesthesia↗
PubMed1988

The combined effects of dopamine (DA) and the DA antagonists EGYT-2509, chlorpromazine and haloperidol on the kidney function.

In anaesthetized dogs renal function was investigated in four successive 20-min periods in four experimental series. (1) In the first series following the first period (serving as control) 2.5 micrograms/kg/min of dopamine (DA) dissolved in 0.5 ml/min of Ringer's solution was infused into the left renal artery (period 2), than during periods 3 and 4. It was found that first (period 2) and second (period 3) doses of DA induced a significant decrease of about 20-30% in renal vascular resistance, and an increase of about 15-25% in renal blood flow. At the same time, systemic arterial blood pressure fell by 10%. The other investigated parameters of the left kidney (Cinulin, CPAH, sodium, potassium and water excretion) did not differ from the respective parameters of the intact right kidney. (2) In the second experimental series following the first period (prior to period 2) 1.0 mg/kg of the DA antagonist EGYT 2509 was administered intravenously. Prior to the period 3 again 1.0 mg/kg of EGYT 2509 and prior to period 4 2.0 mg/kg of EGYT 2509 was given intravenously. During periods 2 through 4 2.5 micrograms/kg/min of DA was infused into the left renal artery. It could be ascertained that EGYT 2509 abolished the renal effects of DA while not inducing any decrease in arterial blood pressure. (3) In the third experimental series, following the control period, prior to periods 2,3 and 4, 1.0 mg/kg, 1.0 mg/kg and 2.0 mg/kg chlorpromazine respectively, was administered i.v. followed by the infusion of DA into the left renal artery. After the administration of chlorpromazine arterial blood pressure and renal vascular resistance fell concomitantly and DA failed to induce any further changes in these parameters. According to our experiments chlorpromazine abolishes the effect of DA on kidney function. (4) In the fourth series, prior to DA infusion the dogs were given 0.5 mg/kg (period 2) then again 0.5 mg/kg and finally 1.0 mg/kg of haloperidol intravenously. Haloperidol decreased arterial blood pressure as well as renal vascular resistance, thus renal blood flow did not change. Renal blood flow could then be increased by DA infused into the left renal artery. It seems that haloperidol could not abolish the vascular effects of DA in the kidney. Our experiments indicate that substance EGYT 2509 possesses the most marked dopaminergic antagonistic effect, chlorpromazine had also been effective, while haloperidol had proved to be practically ineffective.

Animals↗
PubMed1984

A comparison of renal function following the infusion of Ringer solution into systemic and portal veins in the dog.

The increase of sodium and water excretion by the kidney following intravenous Ringer solution infused into a femoral vein (vena femoralis) or into an intestinal vein (vena portae ) has been studied in anaesthetized dogs. The functional parameters of renal function have been compared during volume expansion with 1.5-2.0% of body weight Ringer solution and "over-hydration" by 2.5% Ringer loading over 60 minutes. No significant difference in sodium excretion and urine output resulted from 0.25 ml/kg/min Ringer solution when infused by the two routes. When the animals were infused with 2.5% body weight Ringer solution (0.66 ml/kg/min i.v.), a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hyposmotic as compared with the plasma osmolarity. No difference has been found in the glomerular filtration rate and in the PAH clearance. Glomerular filtration rate, sodium excretion and urine flow rate were not significantly different for the two routes when the same Ringer solution load was infused. These experiments did not provide evidence for the participation of the liver in the control of sodium excretion during extracellular fluid volume expansion induced by Ringer solution infusion.

Animals↗
PubMed1983

Inhibition of prostaglandin synthesis and the action of vasopressin during extracellular volume expansion in the dog.

The increased renal sodium and water excretion after an intravenous infusion of Ringer solution has been investigated in anaesthetized dogs. The response of the kidneys has been examined in four combinations. The functional parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution and overhydration by 2.5% Ringer solution for 60 min. In the control animals, volume expansion by 2% body weight Ringer solution resulted in a significant increase in sodium excretion and urine flow. When these animals were infused with 2.5% body weight Ringer solution a marked increase in water excretion was observed with a smaller increment in sodium excretion, and the urine became hypo-osmotic as compared to the plasma. No difference was found in glomerular filtration rate and PAH clearance. In the group No. 2, the effect of 4 mg/kg indomethacin infusion was studied. The inhibition of prostaglandin synthesis considerably reduced the diuretic effect of Ringer infusion and did not affect sodium excretion. In the group No. 3, the animals received lysine-8-vasopressin i.v. in a preliminary dose of 10 mU/kg during 10 min and then 50 mU/kg over 60 min in infusion. Volume expansion with 2.5% body weight of Ringer solution resulted in a marked increase in sodium and water excretion but no difference was found in glomerular filtration rate and PAH clearance. Dilution of the urine i.e. a decrease of urinary osmolarity, in spite of the vasopressin infusion, was significantly higher in this group than in the control animals (group No. 1). In the fourth series, after 4 mg/kg of indomethacin the same dose of vasopressin was administered as in group No. 3. Indomethacin was observed to inhibit the diuretic effect of vasopressin and did not affect the saluretic effect. From these data it was concluded that medullary tonicity affected renal water handling during extracellular isosmotic hypervolaemia induced by Ringer infusion. This mechanism depends on medullary prostaglandin synthesis and is independent from the plasma vasopressin concentration. Our findings clearly indicate that extracellular hypervolaemia increases renal sodium excretion and lysine-8-vasopressin was found to potentiate this effect. This sodium excretion increasing mechanism does not depend on renal prostaglandin secretion, nor were glomerular factors responsible for the increase of sodium and water excretion.

Animals↗
PubMed1982

Influence of augmentation of excretory renal mass on renal function after alpha-receptor blockade.

The effect of renal function of an augmentation of the excretory renal mass was investigated in 10 dogs without drug treatment and in 10 animals with alpha-receptor blockade. In the untreated group, augmentation of excretory renal mass by transplantation into the neck of one pair of kidneys isolated from another animal caused the following changes in the kidneys in situ: marked elevation in CPAH, slight decrease in Cinulin, slight diminution of urine excretion and a pronounced fall in sodium excretion. The amount of urine and sodium excreted by the four kidneys was identical with that previously excreted by the two kidneys in situ. In animals with alpha-receptor blockade, augmentation of the excretory renal mass had the following consequences in the in situ kidneys, CPAH, and Cinulin remained unchanged while urine and sodium excretion decreased to the same extent as in the untreated control group. The amount of urine and of sodium excreted by the four kidneys was the same as that excreted by the kidneys in situ, prior to transplantation of isolated kidneys, i.e. before the augmentation of excretory renal mass. It seems that the decrease in sodium excretion of the kidneys in situ was not due to the haemodynamic changes evoked by the load on the circulation; it was rather consequence of some quick, presumably humoral, regulation. The diminution of sodium excretion in the kidneys in situ after augmentation of the excretory renal mass has been ascribed to an increased utilization by the four kidneys of the natriuretic factor(s), i.e. to a diminution in the plasma level of the natriuretic hormone.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of indomethacin on renal function during different levels of surgical stress.

To determine whether renal prostaglandins participate in the regulation of renal blood flow, sodium and water excretion during "stress situation", renal function was investigated in two groups of anaesthetized dogs, subjected to minor and to more severe surgical stress under control conditions, and following the administration of 4 mg/kg indomethacin i.v. In the control studies, the renal haemodynamic parameters (CPAH, Cinulin), urine output and sodium excretion were not different in those animals in which the surgical traumatization was more severe from data obtained in similarly anaesthetized dogs. Extracellular volume expansion induced with i.v. infusion of Ringer solution enhanced sodium and water excretion in both groups, however, the increase of sodium excretion was less in the dogs subjected to more severe stress. During indomethacin infusion glomerular filtration did not change in either groups; CPAH decreased by 20-25% in the anaesthetized animals and 35-40% in dogs in which the surgical stress was more severe. In this group the total renal blood flow was reduced by 40% simultaneously with the haemodynamic changes; sodium and water excretion fell in both groups. After indomethacin infusion the diuretic response of the kidneys to extracellular volume expansion was markedly reduced in the anaesthetized dogs, the diuretic and natriuretic effects being almost completely inhibited in the animals subjected to more severe stress. These data suggest that in the anaesthetized dog endogenous prostaglandins may serve to maintain renal blood flow but not the glomerular filtration rate. Inhibition of prostaglandin synthesis during more severe stress results in increased renal vascular resistance and reduced renal blood flow. Accordingly, the data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during more severe surgical traumatization. The data do not support the direct physiological role of prostaglandins in regulating tubular function.

Animals↗
PubMed1982

Study of the indomethacin and bradykinin antagonism in anaesthetized dogs.

To determine the prostaglandin dependent and independent effects of bradykinin in the kidney, bradykinin (0.05 microgram/min/kg body weight) was infused into the left renal artery during inhibition of prostaglandin synthesis by indomethacin. Indomethacin, 0.1 mg/min/kg body weight i.v. produced a marked fall in urine output and sodium excretion in anaesthetized dogs. Renal vascular resistance increased and renal blood flow (RBFdir) decreased by 30%. When during the i.v. infusion of indomethacin bradykinin was infused into the left renal artery, RBFdir, urine flow and sodium excretion increased to the control values in the left kidney while remained lower in the right kidney. The results suggest that bradykinin increases renal blood flow by an action which does not require the mediation of prostaglandins. A decrease in renal blood flow, which was a constant feature during i.v. indomethacin infusion, is probably responsible for the decrease in urine flow and sodium excretion. The failure of indomethacin to inhibit the natriuretic and diuretic effects of bradykinin suggests that the prostaglandins are not important determinants of these responses.

Animals↗
PubMed1980

The effect of indomethacin on renal function.

The effect of indomethacin on the renal function has been surveyed by the literature and our experimental data. The primary purpose of the present paper is to discuss the various mechanisms of the prostaglandins which participate in the overall operation of the kidney. Prostaglandin has been proposed as a "natriuretic hormone" effecting the natriuresis observed with extracellular fluid volume expansion. Dogs and rabbits were volume expanded under Nembutal anaesthesia. The massive natriuresis associated with expansion ws significantly reduced in dogs by preloading injection of indomethacin (4 mg/kg) to depress prostaglandin synthesis. The indomethacin pretreatment considerably increased the diuretic and natriuretic effect of the volume expansion in the rabbit. The data are consistent with the concept that intrarenal prostaglandins play a role in adjustment of renal vascular resistance and support the concept of a physiological role of intrarenal PG-s in regulating salt and water excretion.

Animals↗