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Biomedical subjects

D Rodríguez-Puyol

Publications and source records attributed to D Rodríguez-Puyol.

53 records · Page 3Linked to original sources
PubMed1993

Somatostatin antagonizes angiotensin II effects on mesangial cell contraction and glomerular filtration.

The effects of somatostatin (ST) on the regulation of the glomerular filtration rate have not been extensively studied. The present experiments were designed to analyze this possible relationship. ST alone did not modify the planar cell surface area (PCSA) of cultured rat mesangial cells (CRMC), but it prevented and reversed the reduction in PCSA induced by 10 nM angiotensin II (Ang II) in a dose- and time-dependent manner. ST (1 microM) completely prevented and reversed the increase in the myosin light chain phosphorylation induced by 10 nM Ang II. Incubation with pertussis toxin (PT, 0.5 micrograms/ml) inhibited the effect of ST on the Ang II-dependent changes in PCSA, but this effect was not inhibited by the blockade of the vasodilatory prostaglandins (indomethacin, 10 microM) or nitric oxide (L-N-methyl-arginine, 0.2 mM) synthesis. 2',5'-dideoxyadenosine (DDA, 0.1 mM), an adenylate cyclase blocker, and methylene blue (MB, 30 microM), a soluble guanylate cyclase blocker, did not interfere with the ST inhibitory effect on the Ang II-dependent reduction in PCSA of rat mesangial cells. ST also blocked the reduction in PCSA induced by phorbol myristate acetate (PMA, 300 nM). ST was also able to prevent and revert the Ang II dependent reduction in glomerular cross-sectional area of isolated rat glomeruli, also in a dose- and time-dependent fashion. Finally, intravenous administration of ST (200 ng/kg body wt as a bolus plus a continuous injection of 25 ng/min/kg body wt) partially blocked the reduction in GFR (measured as CIn) and RPF (measured as CPAH) and the increase in filtration fraction induced by the intravenous administration of Ang II (1.7 micrograms/min/kg body wt) in anesthetized rats. In summary, these results suggest that ST could antagonize the renal actions of Ang II, increasing the GFR and RPF decreased by Ang II, and this effect could be dependent, at least partially, on a direct relaxing effect of ST on mesangial cells.

Adenylate Cyclase Toxin↗
PubMed1993

Changes in renal function in acute experimental pancreatitis in rats: a therapeutic role for somatostatin.

1. The present study was designed to determine the changes in renal function in two models of experimental pancreatitis in rats, in an attempt to assess the possible pathogenic role of reactive oxygen species and to elucidate a possible therapeutic role for somatostatin. 2. Mild pancreatitis was induced by low blockade of the biliary duct and severe pancreatitis was evoked by retrograde infusion of bile salts. Renal function was studied by clearance techniques in rats with pancreatitis, treated or not treated with somatostatin. Plasma and glomerular malonyldialdehyde levels were measured by the thiobarbituric acid method. 3. Renal function did not change in rats with low blockade of the biliary duct, but animals receiving a retrograde infusion of bile salts showed a significant decrease in glomerular filtration rate and renal plasma flow with respect to sham-operated animals. 4. Plasma malonyldialdehyde levels increased significantly in rats treated with bile salts with respect to control animals, whereas no changes were detected in glomerular malonyldialdehyde levels. Thus, the renal dysfunction does not seem to be related to an increased production of reactive oxygen metabolites at the glomerular level. 5. Somatostatin infusion significantly improved renal function in rats with severe pancreatitis (retrograde infusion of bile salts) by increasing glomerular filtration rate, renal plasma flow and filtration fraction. These results support a possible therapeutic role for somatostatin in the renal dysfunction associated with the severe forms of pancreatitis.

Acute Disease↗
PubMed1992

Effects of reactive oxygen species on cultured rat mesangial cells and isolated rat glomeruli.

The effects of reactive oxygen species (ROS) on cultured rat mesangial cells were studied by measuring planar cell surface area (PCSA) after incubation with xanthine plus xanthine oxidase (XXO), in the presence of superoxide dismutase (SOD; 5 micrograms/ml) or catalase (CAT; 20 micrograms/ml), or after incubation with H2O2. Myosin light chain (MLC) phosphorylation was assessed in cells prelabeled with o-[32P]phosphoric acid and incubated with H2O2, after protein separation with sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A possible intermediate role for platelet-activating factor (PAF) was analyzed by preincubation of the cells with a PAF antagonist BN 52021 (BN, 5 x 10(-5) M) and by measuring PAF-specific [3H]acetate incorporation and immunoassayable PAF. XXO significantly decreased PCSA (14%), an effect abolished by CAT but not by SOD. H2O2 induced a similar effect, in a dose-dependent and time-dependent manner. MLC phosphorylation increased by 81 +/- 15% after H2O2 incubation, and this effect was blocked by BN. BN also completely blocked the effect of H2O2 on PCSA. PAF-specific [3H]acetate incorporation increased in the presence of H2O2 (from 6,886 +/- 2,030 to 58,703 +/- 16,063 counts.min-1.mg-1) as well as the immunoassayable PAF production by cells (from 0.90 +/- 0.19 to 6.71 +/- 2.27 ng/mg). These results suggest that ROS, particularly H2O2, could modulate the surface area of mesangial cells, modifying the ultrafiltration coefficient, thus explaining the decrease in glomerular filtration rate in those pathological situations characterized by an increased ROS synthesis. PAF could be involved in the genesis of these effects.

Animals↗
PubMed1990

Cellulose acetate membrane improves some aspects of red blood cell function in haemodialysis patients.

The present study was designed to evaluate the influence of two haemodialysis membranes of different biocompatibility on red blood cell function. Twelve patients were studied in two consecutive dialyses, with cuprophan and cellulose acetate. Blood was extracted at 0, 20 and 180 min after the beginning of the haemodialysis session and general haematological parameters, osmotic fragility, deformability, methaemoglobin concentration and malonyldialdehyde (MDA) red blood cell content were determined. Osmotic fragility improved with both membranes, but this improvement was more marked with cellulose acetate. MDA red blood cell content showed a tendency to increase after 3 h with cuprophan (114 +/- 11% of the basal value), whereas it tended to decrease with cellulose acetate (92 +/- 12%), the differences between the two groups being statistically significant. These results suggest that red cell function may improve by changing the characteristics of haemodialysis membranes. This phenomenon could be related to a better biocompatibility.

Adult↗
PubMed1989

Actions of cyclosporin A on cultured rat mesangial cells.

The effects of cyclosporin A (CsA) on planar surface area of cultured rat mesangial cells (PCSA) and cross-sectional area of isolated rat glomeruli (GCSA) were tested. The same experiments were performed after preincubation with platelet activating factor (PAF) antagonists (BN 52021, alprazolam) or calcium channel blockers (verapamil). Areas of cells or glomeruli were analyzed by a computer-assisted method. CsA reduced PCSA in a time-dependent (significant effects began at 15 min, about 12% of reduction with 10(-6) M CsA) and dose-dependent (no effect at 10(-9) M CsA, maximal reduction of about 30% at 60 min of incubation with 10(-7) M CsA) fashion. BN 52021 (5.10(-5) M) and alprazolam (10(-5) M) completely inhibited the reduction of mesangial cell area induced by CsA. Verapamil (10(-5) M) only partially inhibited this action. Glomerular cross-sectional area decreased after 30 minutes of incubation with 10(-6) M CsA (1.45 +/- 0.02 vs. 1.55 +/- 0.02 m2.10(-8), P less than 0.001), an effect that was inhibited by BN 52021 or verapamil. In addition, 10(-6) M CsA increased PAF production by isolated rat glomeruli (425 +/- 80 pg/mg vs. 198 +/- 13 pg/mg in control glomeruli, P less than 0.01), an effect which was not inhibited by verapamil. These results suggest that CsA could reduce GFR by decreasing the glomerular ultrafiltration coefficient, perhaps as a consequence of the contraction of mesangial cells. PAF seems to play a pivotal role in the genesis of this action.

Animals↗
PubMed1988

Urinary excretion and glomerular synthesis of prostaglandin E2 and prostaglandin F2 alpha in cirrhotic, non-ascitic rats: the effects of sodium overload.

The urinary excretion of aldosterone, kallikrein and prostaglandin E2 (PGE2) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE2 was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE2. Isolated glomeruli of RC rats produced less PGE2 than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.

Aldosterone↗
PubMed1988

Plasma catecholamines and urinary excretion of their main metabolites in three models of portal hypertension.

We have measured, by a specific radioenzymoassay, the plasma concentration of dopamine (DA) and norepinephrine (NE) and by gas chromatography the urinary excretion of some catecholamine metabolites (HVA, homovanillic acid, DOPAC, dihydroxyphenyl acetic acid; VMA, vanilmandelic acid, and DOPEG, dihydroxyphenyl glycol) in three groups of rats with portal hypertension: cirrhotic rats (CR), rats with progressive portal hypertension (PPH) and rats with progressive hepatic congestion (PHC). The three groups of rats had portal hypertension. PPH and PHC had also intrahepatic hypertension. CR rats showed an increased urinary excretion of NE and DA metabolites with a normal plasma concentration of these catecholamines, suggesting an increased turnover of NE and DA in this experimental model. PPH animals had a high plasma DA concentration with a decreased urinary excretion of catecholamine metabolites. PHC showed high plasma DA and NE levels with normal or increased urinary excretion of its metabolites. These results suggest that an increased neural activity is present in the early stages of experimental cirrhosis in rats and this alteration does not seem directly related to the portal hypertension but perhaps to the intrahepatic hypertension or to the hepatocellular damage.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Atrial natriuretic peptide inhibits glomerular contraction induced by angiotensin II and platelet activating factor.

Isolated rat glomeruli were incubated with angiotensin II, PAF and atrial natriuretic peptide (ANP). Angiotensin II and PAF produced a significant glomerular contraction as evidenced by the decrease in glomerular cross-sectional area. The addition of ANP abolished this effect. These results suggest that ANP could modulate glomerular filtration rate, not only by inducing changes in intrarenal hemodynamics, but also by preventing the effect of some hormones on the filtration surface and subsequently on the ultrafiltration coefficient.

Angiotensin II↗
PubMed1987

Changes in glomerular cross-sectional area induced by platelet activating factor.

Isolated glomeruli from normal rats were incubated with platelet-activating factor 10(-6) M at variable incubation times (8, 15, 30 and 45 min) and with different concentrations (0 to 10(-6) M) for 20 min. In addition, the platelet-activating factor effect (10(-6) or 10(-8) M, 20 min) was tested in the presence of BN-52021 (10 or 50 micrograms/ml), verapamil (10(-5) M), acetylsalicylate of lysine (10(-3) M), and in a free-calcium media with EGTA 2 mM. Glomerular microphotographs were taken before and 20 min after adding the substances, and glomerular cross-sectional area was measured using a computerised technique. Platelet-activating factor induced a significant time-dependent reduction in glomerular cross-sectional area, from a concentration of 10(-8) M. BN-52021, verapamil, and the free-calcium media inhibited platelet-activating factor-induced reduction of glomerular cross-sectional area, but acetylsalicylate of lysine did not. Platelet-activating factor-induced reduction in glomerular cross-sectional area seems to be dependent on the interaction of platelet-activating factor with a specific glomerular receptor, with a subsequent modification of the intracellular concentration of calcium. Arachidonic acid metabolites from the cyclo-oxygenase pathway do not seem to be involved in these phenomena. Results suggest that platelet-activating factor could modulate glomerular filtration rate not only by inducing changes in systemic or intrarenal haemodynamics, but also by modifying the filtration surface, thus reducing the Kf.

Animals↗
PubMed1986

Lack of a direct regulatory effect of atrial natriuretic factor on prostaglandins and renin release by isolated rat glomeruli.

We have tested the direct regulatory effect of synthetic Atrial Natriuretic Peptide (ANP, 8-33aa) on prostaglandins and renin release by isolated rat glomeruli. Variable incubation times and doses of ANP did not modify the rate of PGE2, PGF2a and TXB2 production. Similar results were obtained for renin release. These data do not support a role for ANP in the regulation of prostaglandins and renin release by rat glomeruli.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Molecular heterogeneity of circulating prolactin in chronic uremic men and renal transplant recipients.

Serum PRL levels and its molecular heterogeneity were analyzed, basally and after 500 micrograms TRH given acutely, in four groups of men: normal (C, n = 12), chronic renal failure (CRF, n = 11), hemodialysis (HD, n = 12), and transplant recipients (T, n = 11). The mean basal PRL level was higher in group CRF than in group C and even higher in group HD. The basal hyperprolactinemia was due to increased concentrations of little PRL. The absolute levels of total and little PRL 20 min after TRH were comparable in the four groups. The disappearance index (DI = PRL20-PRL120/PRL20) for total and little PRL was lower in CRF than in C and even lower in HD. A positive correlation was found between the DIs of total and little PRL and creatinine clearance in group CRF. Group T had basal and 20 min serum PRL levels and a pattern of molecular distribution similar to those of group C but total and little PRL DI was lower. These results demonstrate that uremic hyperprolactinemia is due to increases in little PRL without major changes in big and big-big forms of PRL. The reduction of glomerular filtration rate seems to be one of the most important mechanisms responsible for little PRL accumulation.

Adult↗
PubMedDate not supplied

Parathyroid hormone-related protein: roles in the glomerulus.

Parathyroid hormone (PTH) and PTH-related protein (PTHrP) produce similar biological effects through the PTH/PTHrP receptor. Less is known about the physiological role of PTHrP which was first identified as the agent of the humoral hypercalcemia of malignancy. Despite the widespread production of PTHrP in healthy individuals, the concentration of the protein is below the detectable limit of current assays, suggesting that PTHrP normally functions locally in an autocrine or paracrine manner. Thus, some differences in their biological activities have been described, and they may be related to the presence of different receptors. In this regard, a second receptor which binds selectively to PTH has also been found. Recent studies have demonstrated the expression of both PTH/PTHrP receptor and protein in the renal glomeruli. Moreover, there are convincing data that support a direct role of PTH and PTHrP in modulating renal blood flow and glomerular filtration rate. This multifunctional protein, PTHrP, also has a proliferative effect on mesangial cells, supporting the notion that it may play a role in the normal glomerulus and in injured kidney.

Animals↗
PubMedDate not supplied

Phenotypic modifications of human mesangial cells by extracellular matrix: the importance of matrix in the contractile response to reactive oxygen species.

The progression of chronic renal diseases is characterized by the accumulation of extracellular matrix proteins in the glomerulus. The present experiments were designed to analyze the effect of hydrogen peroxide on the contractile and proliferative phenotypes of human mesangial cells grown on different culture substrates: plastic, collagen type I, and collagen type IV. Contraction was analyzed by measuring planar cell surface area and myosin light chain phosphorylation, whereas proliferation was studied by [(3)H]thymidine incorporation. No changes were detected in the proliferation rate of human mesangial cells grown on different culture substrates, neither under basal conditions nor in the presence of fetal calf serum or H(2)O(2). Cells grown on plastic or collagen did not contract in the presence of H(2)O(2), but cells grown on collagen I elicited a significant contraction with H(2)O(2). Platelet-activating factor induced contraction of human mesangial cells on the three culture substrates. The different contractile responses observed were not due to different degradation rates of H(2)O(2). The present experiments support the importance of extracellular matrix in the response to exogenous stimuli and point to the possibility that patients with changes in the mesangial matrix as a result of chronic renal diseases may have an increased susceptibility to the pathological actions of reactive oxygen species.

Cells, Cultured↗