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Biomedical subjects

J Uranga

Publications and source records attributed to J Uranga.

At least 19 recordsLinked to original sources
PubMed1991

Enhanced glomerulopressin production and glomerular filtration rate by amino acid infusion in normal humans.

Amino acid infusion induces a rise in glomerular filtration rate (GFR) in normal subjects, but the mechanism is as yet unknown. Glomerulopressin infused into the renal arteries of rats and dogs increases GFR. The aim of this study was to ascertain whether amino acid infusion raised glomerulopressin production and GFR. Accordingly, before renal arteriovenography, in 11 potential kidney donors, the caval catheter was introduced into the right hepatic vein and 60-ml blood samples were collected at the beginning and end of each experiment; six patients received amino acid infusion and five a saline infusion. Glomerulopressin in ultrafiltrates from hepatic vein plasma was measured by toad bioassay and GFR determined with diethylenetriamine pentaacetic acid-Tc99. The amino acid-infused group showed significant glomerulopressin activity in ultrafiltrates, as well as a significant GFR increase, whereas in the control group no glomerulopressin activity was observed, and there was no change in GFR. These findings suggest that intravenous amino acid infusion stimulates glomerulopressin production, which may in turn induce an increase in GFR.

Adult↗
PubMed1991

Glomerulopressin production by isolated rat liver after amino acid infusion.

The infusion of certain amino acids, such as serine, alanine, and proline (SAP), has been shown to increase the glomerular filtration rate, whereas branched chain amino acids (BCAA) leucine, isoleucine, and valine fail to modify the glomerular filtration rate. It has been suggested that this effect of amino acids on the glomerular filtration rate is mediated by the action of the hormone glomerulopressin. The purpose of this work was to study the action of SAP and BCAA on glomerulopressin production. Livers isolated from rats were perfused with (i) Krebs-Ringer-Bicarbonate, (ii) SAP, or (iii) BCAA. Results indicate that glomerulopressin production is stimulated by SAP, but inhibited by BCAA.

Alanine↗
PubMed1987

Purification of glomerulopressin.

The present investigation was undertaken to attempt the purification of glomerulopressin. Isolated rat livers were perfused with Krebs-Ringer bicarbonate, and the perfusate was concentrated at reduced pressure, extracted with n-butanol, and subjected to thin-layer chromatography (TLC) with different solvent systems. For monodimensional TLC, (a) acetic acid or (b) chloroform/methanol/formic acid (65:30:5, v/v) was used. For bidimensional TLC solvent (b) was used as the first mobile phase and as the second mobile phase three different solvent systems were employed as follows: ethyl acetate/n-butanol/formic acid (40:57:3; v/v), pyridine/methanol/formic acid (50:49:1, v/v), and acetic acid/n-butanol/water (5:50:10, v/v). The activity of the spots viewed under uv light was studied in three different biological assays: increase of the glomerular pressure index (GPI) in the toad and of the glomerular filtration rate (GFR) in the rat and increase of the tonic tension contraction in the rat stomach strip (TTC). In monodimensional TLC developed with system (a), three spots were detected, and with system (b), seven spots were observed. The biological activity of these seven spots was studied. Only the substance showing Rf 0.47 was active. This Rf 0.47 spot subjected to bidimensional TLC with the three different solvent systems moved in the second direction as only one spot. To confirm whether the Rf 0.47 spot was composed by only one substance, reverse-phase HPLC was performed in a Waters radial compression unit using three different elution systems and in a Hewlett-Packard model equipped with an ultrasphere ODS column. With these different HPLC columns and elution systems, only one peak was observed. This is the first attempt to purify a substance showing a biological activity similar to that of glomerulopressin.

Animals↗
PubMed1987

Effect of glomerulopressin on several isolated veins and arteries of different species.

The effect of glomerulopressin was investigated in several isolated veins and arteries of dog and also in veins of rabbit, rat, and hamster. Glomerulopressin contracted some of the dog veins: jugular, extrahepatic porta, femoral, cava, iliac, splenic, and had no effect in pulmonary, mesenteric, and renal vein. It was also active in some dog arteries: Iliac, femoral, renal, and had no effect in aorta, hepatic, splenic and pulmonary artery. In the rat it increased the frequency of the spontaneous rhythmic contraction of the extrahepatic porta. No effect was observed in any of the rabbit veins assayed: cava, jugular, iliac and extrahepatic porta, nor in the extrahepatic portal vein of the hamster. In another group of experiments, inhibitors of phospholipase A2, chlorpromazine and mepacrine were added to the bath. These inhibitors blocked the effect of glomerulopressin in the three dog vessels that were assayed: jugular, extrahepatic porta and iliac artery. These results show that glomerulopressin induces a contraction in several, but not all, veins and arteries, and that its effect is mediated by the liberation of arachidonic acid.

Animals↗
PubMed1986

Glomerulopressin activity in peripheral blood of newly diagnosed type I (insulin-dependent) diabetic patients and in normal subjects treated with glucagon.

The glomerulopressin activity of the ultrafiltrate obtained from the peripheral blood of normal subjects, newly diagnosed Type I (insulin-dependent) diabetic patients (IDD), and in normal subjects treated with glucagon was studied in two bioassays: tonic tension contraction of the rat stomach fundus (TTC) and increase in the ureteral pressure of the toad, which was considered as a glomerular pressure index (delta GPI). The ultrafiltrate of four normal volunteers had a low activity in the TTC assay, and in two subjects no activity was observed. The ultrafiltrate of five of these subjects had no activity in delta GPI. In IDD patients the ultrafiltrates were active in the TTC assay and in the toad assay. In glucagon treated normal volunteers three of the ultrafiltrates were very active in the TTC assay and other three had a low activity. In the toad assay five of them were active and no response was observed in one subject. These observations suggest that glomerulopressin activity is increased in peripheral venous blood of untreated newly diagnosed IDD patients and in normal subjects treated with glucagon.

Adolescent↗
PubMed1985

Induction of glomerulopressin production by cyclic AMP.

Isolated rat livers were perfused with gassed Krebs-Ringer-Bicarbonate and different doses of theophylline and dibutyryl cyclic AMP were added to the perfusing solution. The perfusates were ultrafiltrated through Diaflo UM-05 membranes. The glomerulopressin activity of the ultrafiltrates were assayed in the tonic tension contraction (TTC) of isolated stomach fundus from rats. As glomerulopressin is known to be a glucuronide, it was inactivated with beta-glucuronidase to confirm that the effect on the stomach fundus was due to the glomerulopressin and not to another substance. It was observed that doses of theophylline between 2 x 10(-3) M and 2 x 10(-5) M enhanced glomerulopressin production. However, there was no relationship between dose of theophylline and the response, and a dose of theophylline 2 x 10(-6) M has no activity. The perfusion with dibutyryl cyclic AMP at 5 x 10(-8) M increased the amount of glomerulopressin produced by the liver. This was a log-dose response of glomerulopressin production to dibutyryl cyclic AMP between 5 x 10(-8) M and 5 x 10(-4) M. Theophylline (2 x 10(-6) M) potentiated the activity of cyclic AMP (5 x 10(-8) M). These results support the view that cyclic AMP is intracellular mediator of the hepatic production of glomerulopressin.

Animals↗
PubMed1985

Isolated dog coronary arteries response to glomerulopressin.

Coronary arteries were excised from pentobarbital anesthetized normal dogs. The isolated coronary arteries were placed in an oxigenated KRB bathing solution maintained at 37 degrees C and pH 7.4 changes in the basal tone were measured. The addition of glomerulopressin to the bathing solution produced a decrease of 26 +/- 1.5 mg of the basal tone. This decrease was prolonged for more than 40 minutes. Several inhibitors of prostaglandins synthesis were added to the bath such as corticosterone (2 X 10(-5) M), indomethacin (6 X 10(-6) M), acetylsalicylic acid (1.8 X 10(-4) M) and tranylcypromine (4 X 10(-4) M). All these inhibitors blocked the action of glomerulopressin. We conclude that glomerulopressin relaxes the coronary arteries and that this relaxation may be mediated through the novobiosynthesis of prostaglandins.

Animals↗
PubMed1982

Influence of insulin and glucagon on the production of glomerulopressin by isolated rat liver.

Isolated rats livers were perfused with Krebs-Ringer-Bicarbonate (KRB) and different doses of insulin or glucagon and with insulin plus glucagon. The isolated liver of fasted rats and of rats treated with streptozotocin were perfused with (KRB). The glomerulopressin activity of the ultrafiltrate of the liver perfusates were assayed in the tonic tension contraction (TTC) of isolated stomach fundus from rats. As glomerulopressin is known to be a glucuronide, it was inactivated with beta-glucuronidase to confirm that the effect on the stomach fundus was due to the glomerulopressin and not to an autacoid. It was observed that glucagon increased the glomerulopressin activity of the perfusate and that this activity was independent of the dose of glucagon used. Insulin produced a decrease in the glomerulopressin activity of the perfusate, there being a log-dose relationship between insulin and glomerulopressin. There is a dose of insulin (1,5 X 10(-5) U/min/kg) that potentiates the response to glucagon. Fasting and treatment with streptozotocin induced an increase in the glomerulopressin activity of the perfusate. These results suggest that glomerulopressin production is influenced by glucagon and insulin, and that there is a specific ratio between these hormones that is very effective in the production of glomerulopressin.

Animals↗
PubMed1982

Some factors affecting glomerulopressin production by perfused rat liver.

Studies were carried out on the production of the glucuronide hormone glomerulopressin by the isolated rat liver in male and female rats, and the effect on this production of an inhibitor (Novobiocin) and a stimulator (benzo-(a)pyrene) of glucuronyltransferase activity. It was observed that males produce more glomerulopressin than females, Novobiocin inhibits its production while benzo-(a)pyrene enhances it in females but not in males. The changes in glomerulopressin production are related to the changes in glucuronyltransferase activity observed by other authors, suggesting that this enzyme is involved in the production of glomerulopressin.

Animals↗
PubMed1982

Influence of corticoids on the production of glomerulopressin by isolated rat liver.

The isolated liver of rats treated with dexamethasone, hydrocortisone, and deoxycorticosterone acetate (DOCA) was perfused with Krebs-Ringer Bicarbonate (KRB). The liver of adrenalectomized rats was also perfused with KRB. The glomerulopressin activity of the ultrafiltrate of the liver perfusates was assayed in the tonic tension contraction (TTC) of isolated stomach fundus from rats. As glomerulopressin is known to be a glucuronide, it was inactivated with beta-glucuronidase to confirm that the effect on the stomach fundus was due to the glomerulopressin and not to an autacoid. It was observed that dexamethasone, hydrocortisone and DOCA inhibit glomerulopressin production, but adrenalectomy had no effect, therefore it can be deduced that the adrenals are not necessary for the production of glomerulopressin.

Adrenalectomy↗
PubMed1980

Effect of glomerulopressin and mannitol in acute renal failure in rats.

Glomerulopressin is a hormone that increases glomerular filtration rate (GFR) in toads, rats, and dogs. In this study, the effect of glomerulopressin was assayed in two models of acute prerenal failure, by haemorrhage and by partial occlusion of the aortic artery. In animals with 30 min of anuria both mannitol and glomerulopressin increased GFR and urinary flow, but if the rats were anuric for 120 min, only glomerulopressin was effective in restoring GFR and urinary flow. Glomerulopressin also restored GFR and urinary flow in animals that had remained anuric for 24 hours.

Acute Kidney Injury↗
PubMed1979

Effect of glucagon and glomerulopressin on the renal function of the dog.

Glucagon was infused through the porta or through the left renal artery in dogs. Another group of dogs were infused with glomerulopressin through the left renal artery. It was observed that glucagon when infused through the portal vein enhanced the glomerulopressin production and the glomerular filtration rate (GFR). When glucagon was infused intrarenally it did not alter GRF but it had a direct tubular action decreasing sodium reabsorption in the proximal tubule. Glomerulopressin infused intrarenally increased GRF and potassium excretion. The results suggest that the increase in GFR was due to increase in glomerulopressin activity. There are three reasons for this statement: a) GRF increased when glomerulopressin activity was high, but not when there was a low activity, 5) intrarenally infused glomerulopressin produced a very significant change in the GFR of the infused kidney, while the GRF of the contralateral kidney remained unchanged and c) intrarenally administered glucagon had no effect on GFR.

Animals↗
PubMed1979

Effect of glomerulopressin on ovarian blood flow in dogs.

The present study showed that glomerulopressin decreased ovarian blood flow in normal dogs and that this effect could be inhibited by treatment with indomethacin. In addition diabetic dogs had a high plasma level of glomerulopressin and a low ovarian blood flow that was shown to increase after treatment with indomethacin. This suggests that the low ovarian blood flow in diabetis might be due to a prostaglandin synthesizing effect of glomerulopressin.

Animals↗
PubMed1979

Action of glomerulopressin on smooth muscle contraction, probably mediated by the release of prostaglandins.

The effect of glomerulopressin on the increase of the contractile tension developed by isolated strips of stomach fundus, duodenum and bladder of rats, was investigated. Glomerulopressin is a glucuronide whose contractile inducing effect was destroyed by beta-glucuronidase. It was observed that glomerulopressin increases the contractile tension of these tissues, and that this action was not blocked by atropine, cyproheptadine, tranylcypromine, but was inhibited by indomethacin, suggesting that the effect of glomerulopressin action was mediated by prostaglandin release.

Animals↗
PubMed1978

Effect of glucagon on glomerulopressin production in diabetic dogs.

Glucagon (21.5 +/- 0.23 ng/min/kg) was infused through the portal vein of normal or pancreatectomized dogs. It was observed that a dose of glucagon that produces no significant change in the glycemia of normal dogs has a very small activity in the production of glomerulopressin and does not alter glomerular filtration rate (GRF). In pancreatectomized dogs this same dose of glucagon also does not alter glycemia but it induces a large increase in the production of glomerulopressin and GFR. Our results suggest that in pancreatectomized dogs glomerulopressin production is more sensitive to glucagon infusion than in normal dogs.

Animals↗
PubMed1977

Increased glomerular filtration rate and glomerulopressin activity in diabetic dogs.

Studies of the chemical characteristics of glomerulopressin were carried out, and the results suggest that glomerulopressin is a glucuronic acid conjugate. Glomerulopressin activity, glucuronide concentration and glomerular filtration rate (GFR), plasma volume (PV), extracellular volume (ECV) and estimated hepatic plasma flow (EHPF), were measured in normal dogs, infused with saline or glucose and in pancreatectomized dogs infused with saline. Glomerulopressin activity, glucuronide concentration and GFR were also measured in pancreatectomized dogs infused with insulin (150 muU/min/kg) through the portal or femoral vein. The glomerulopressin activity, glucuronide concentration and GFR in glucose-infused normal dogs were similar to those observed in saline-infused animals, while they were greatly increased in pancreatectomized dogs. There was no difference between these three groups in PV, ECV, or EHPF. The infusion of insulin through the portal vein of pancreatectomized dogs reduced glomerulopressin, glucuronides and GFR to the values observed in normal dogs, while the infusion on insulin through the femoral vein did not decrease these levels. The increased glomerulopressin produced by pancreatectomy seems to be due to the lack of insulin reaching the liver. The results suggest that pancreatectomy induced an increase of glomerulopressin activity and that this humoral factor increases GFR.

Animals↗