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Biomedical subjects

C Caramelo

Publications and source records attributed to C Caramelo.

At least 73 records · Page 4Linked to original sources
PubMed1994

Atrial natriuretic peptide and cGMP inhibit Na+/H+ antiporter in vascular smooth muscle cells in culture.

The aim of the present paper was to study the mechanisms of the inhibitory effect of atrial natriuretic peptide (ANP) on the sustained contraction phase of vascular smooth muscle cells (VSMC). Specifically, the potential role of ANP on the Na+/H+ antiporter and Na+ transport systems was investigated. Both ANP and 8-bromo cGMP inhibited 22Na+ uptake and decreased intracellular Na ([Na+]i) in VSMC, an effect that was mimicked by the specific Na+/H+ antiporter inhibitor, hexamethylen amiloride (HMA). The effect of ANP was not additive with HMA, therefore suggesting that both inhibit the same 22Na+ transport pathway. On the other hand, the inhibition of 22Na+ accumulation by ANP was additive with the inhibition by furosemide or bumetanide, thus suggesting that both drugs act on different Na+ exchange systems. In HEPES-buffered medium, ANP, cGMP, and HMA significantly inhibited the AVP-induced intracellular alkalinization, an effect which was associated with significant inhibition of the AVP-induced shape change. In bicarbonate buffered medium, ANP and cGMP decreased the pH level below the baseline after application of AVP, and an inhibition by ANP and cGMP of AVP-induced VSMC shape change was also observed. The recovery of cellular pH after three different types of acid load, namely, ammonium chloride pulse, nigericin clamp and lowering of extracellular pH, was significantly decreased by ANP and cGMP. Taken together, these results indicate that ANP/cGMP inhibit the activity of the Na+/H+ antiporter in VSMC, either in hormone- or pH-stimulated conditions.

Amiloride↗
PubMed1994

Choice of dialysis membrane does not influence the outcome of residual renal function in haemodialysis patients.

It has been recently proposed that haemodialysis membrane choice may influence the maintenance of residual renal function. The aim of the present study was to prospectively analyse the effect of membrane choice on the outcome of renal function in patients entering a chronic haemodialysis programme. Twenty-two patients from four hospitals have been randomly assigned to be dialysed with either polysulphone (PSF)/polyacrylonitrile (PAN) (group A; n = 9), or cuprophane membranes (group B; n = 13). Basal and monthly serum biochemistry, residual creatinine clearance (Ccr) and urine volume (Vu), pharmacological and dialytic treatment, diet, and haemodialysis-related complications were recorded. A significant decrease was observed in the two most relevant variables, i.e. remnant Ccr and Vu, within 3 months of starting haemodialysis, with stabilization during the further follow-up. Such decrease was similar (P NS) for both groups A and B throughout the 9-month observation period. In conclusion, our results suggest that the choice of haemodialysis membrane does not influence the outcome of the residual renal function. Renal function decreased significantly within 3 months on haemodialysis, independently of the type of dialyser membrane.

Acrylic Resins↗
PubMed1994

Effect of atrial natriuretic peptide and calcium antagonists on platelet-activating factor-induced contraction and intracellular calcium mobilization in rat mesangial cells.

We studied the effect of platelet-activating factor (PAF-acether) on rat mesangial cells (MC) and the intracellular mechanisms for PAF-acether-mediated MC activation. Contraction was measured as changes in planar cell surface area (PCSA), and intracellular free calcium concentration ([Ca2+]i) was measured as changes in the signal of the fluorescent indicator fura-2. PAF-acether induced a time- and dose-dependent reduction in PCSA and a dose-dependent increase in [Ca2+]i. Both phenomena were abolished by preincubation of the cells with the PAF-acether-binding blockers L652,731 and BN 52021. TMB-8, an inhibitor of intracellular calcium mobilization, partially inhibited both the reduction in PCSA and the increase in [Ca2+]i, whereas the Ca2+ entry blocker verapamil completely inhibited the reduction in PCSA but only partially blocked the increase in [Ca2+]i. Atrial natriuretic peptide (ANP) produced a dose-dependent inhibition of PAF-acether-induced cell contraction, but its effect was not statistically related to changes in [Ca2+]i. These results show that PAF-acether-induced MC contraction is associated with transient increases in [Ca2+]i, but the relaxing effects of ANP and verapamil may require additional physiologic interactions that involve mechanisms other than the [Ca2+]i transient.

Analysis of Variance↗
PubMed1994

Evidence against transmission of hepatitis C virus through hemodialysis ultrafiltrate and peritoneal fluid.

Hepatitis C virus (HCV) infection is highly prevalent in the chronic renal failure population treated in dialysis units. Transmission of HCV via blood transfusions is becoming an increasing problem, but, nevertheless, the routes by which this transmission occurs are incompletely known. We have searched for the presence of HCV RNA by the polymerase chain reaction (PCR) in serum and dialysis ultrafiltrate in 12 hemodialysis and 5 continuous ambulatory peritoneal dialysis (CAPD) patients, all of whom were HCV-antibody-positive. Serum PCR were positive for HCV RNA in all the cases, whereas PCR performed on samples of hemodialysis ultrafiltrate or peritoneal effluent were always negative for HCV RNA. In addition, 13 patients tested positive for HCV antibodies and 19 out of 32 patients sharing the dialysis monitors with 17 PCR-positive individuals remained negative. From these findings, we conclude that the dialysis ultrafiltrate or peritoneal fluid seems to be an improbable source of HCV dissemination in the dialysis setting. Moreover, a significant group of patients remained HCV-antibody-negative although they shared the same dialysis machine with positive patients. Therefore, the importance of other sources of HCV transmission, namely blood-contaminated material, should be emphasized.

Ascitic Fluid↗
PubMed1994

Serum concentrations of carboxyterminal cross-linked telopeptide of type I collagen (ICTP), serum tartrate resistant acid phosphatase, and serum levels of intact parathyroid hormone in parathyroid hyperfunction.

We have studied the levels of a new biochemical marker of bone resorption, carboxyterminal cross-linked telopeptide of type I collagen (ICTP), in 26 healthy control subjects, 15 patients with primary hyperparathyroidism (PHPT) and 17 patients with secondary hyperparathyroidism (secondary HPT). Levels of ICTP in PHPT and secondary HPT have been correlated with those of serum tartrate resistant acid phosphatase (TRAP), another biochemical marker of bone turnover, and with serum levels of intact parathyroid hormone (iPTH). The ICTP levels of the control group were 2.07 +/- 0.58 micrograms l-1, n = 26, range 1.3-3.2. They were independent of sex and age in the studied age range (30-62 years). The ICTP levels of PHPT patients were 3.5 +/- 3.5 micrograms l-1, mean +/- SD, range 0.5-12.2 micrograms l-1, significantly higher than those of control subjects (p < 0.05). We found a significant linear correlation between values of ICTP and iPTH levels (p < 0.01), between values of ICTP and serum activity of TRAP (p < 0.01) and between iPTH and TRAP levels (p < 0.01) in patients with PHPT. The ICTP levels in patients with secondary HPT were higher than those of patients with PHPT, 46 +/- 37 micrograms l-1, range 12-167 micrograms l-1 (p < 0.001) due to the impaired renal clearance of this peptide. We did not find a significant linear correlation between values of ICTP and iPTH levels in the serum of patients with secondary HPT, although we found a significant correlation between levels of ICTP and levels of TRAP, both biochemical markers of bone turnover.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗
PubMed1994

Clinical usefulness of serum carboxyterminal propeptide of procollagen I and tartrate-resistant acid phosphatase determinations to evaluate bone turnover in patients with chronic renal failure.

We have studied the levels of the biochemical markers of bone formation total serum alkaline phosphatase, osteocalcin (BGP) and carboxyterminal propeptide of type I procollagen (PICP), the levels of the biochemical marker of bone resorption serum tartrate-resistant acid phosphatase (TRAP) and those of intact immunoreactive PTH (iPTH) in 30 patients at different stages of chronic renal failure (CRF), all of them without verifiable hepatopathy, and in 9 patients in hemodialysis with hepatopathy measured by the Knodell index. Sixteen control subjects were also studied. In the group of patients with CRF with or without hepatopathy, the levels of biochemical markers of bone turnover were significantly elevated with respect to those of control patients. We did not find any significant difference in the levels of these parameters between the groups with and without liver damage, in spite of the fact that TRAP and PICP are cleared mainly by the liver. Levels of TRAP and PICP correlated significantly with the other biochemical markers of bone turnover studied. The good relation observed between PICP, TRAP and the biochemical indexes of bone activity and iPTH levels suggests the clinical value of these markers in the follow-up of bone involvement in patients with CRF. On the other hand, the frequent hepatopathy found in patients with CRF does not seem to affect to a significant extent the diagnostic value of PICP and TRAP in this pathology.

Acid Phosphatase↗
PubMed1993

Nitric oxide-generating system as an autocrine mechanism in human polymorphonuclear leucocytes.

Recent data [Lopéz-Farré, Riesco, Moliz, Egido, Casado, Hernando and Caramelo (1991) Biochem. Biophys. Res. Commun. 178, 884-891] revealed that endothelin 1 (ET-1) increases intracellular free [Ca2+] in polymorphonuclear leucocytes (PMN) by a mechanism that can be inhibited by L-arginine. The aim of the present study was to clarify the mechanisms of the interaction between the effects of ET-1 and L-arginine in human PMN. The experimental findings showed that in human PMN: (a) ET-1 and the chemoattractant peptide N-formylmethionyl- leucyl-phenylalanine (fMLP) induce both the metabolism of L-arginine to L-citrulline and cyclic GMP (cGMP) formation; (b) the ET-1-induced cGMP production is inhibitable by the L-arginine antagonist NG-monomethyl-L-arginine, therefore suggesting the involvement of NO; (c) the ET-1- or fMLP-induced NO/cGMP stimulation is critically dependent on the availability of L-arginine; (d) human PMN possess a L-arginine transport system with both Na(+)-dependent and -independent components; (e) the L-arginine transport system in PMN appears to be feedback-regulated by NO/cGMP in ET-1-stimulated conditions, but not under baseline conditions; (f) the L-arginine transport system in PMN is independent of the gamma-glutamyl cycle and is not modified by either ET-1 or fMLP. The L-arginine/NO/cGMP-dependent mechanisms characterized in the present study may be relevant in the regulation of PMN activation in pathophysiological conditions in vivo.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Liver disease patterns in hemodialysis patients with antibodies to hepatitis C virus.

The present study correlated histopathology and diagnostic tests in hemodialysis patients with serologic markers for hepatitis C virus (HCV). Hepatitis C virus infection was found in 65 of 163 patients, as assessed by anti-c100-3 (ELISA 1), anti-c22-3, c33C (ELISA 2), and RIBA 2. Several histopathologic patterns were found in 33 liver samples from HCV-positive individuals: cirrhosis (n = 3), chronic active hepatitis (n = 14), chronic persistent hepatitis (n = 2), isolated hemosiderosis (n = 5), reactive hepatitis (n = 6), and others (n = 3). There was a positive correlation between time from the first aminotransferase peak and histologic damage (P = 0.015). However, the severity of liver disease did not correlate with the intensity of RIBA 2 positivity, mean levels or pattern of aminotransferases elevation, or markers of past hepatitis B virus infection. Moreover, aminotransferases were persistently normal in three patients with severe liver disease and were elevated in 10 patients with only mild changes. In 19 biopsied patients, the presence of plasma HCV RNA was examined by the polymerase chain reaction (PCR), which was positive in 15 of the 19 biopsy specimens. The ability of PCR positivity to predict the histologic severity of the disease was insufficient: four patients with minor liver damage had positive PCR and two patients with significant liver damage had negative PCR. No further correlations of PCR positivity were found with the other biochemical or immunologic markers of HCV infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1993

Enhancement of vascular action of arginine vasopressin by diminished extracellular sodium concentration.

The present study was undertaken to examine the effects of diminished extracellular sodium concentration on the vascular action of arginine vasopressin (AVP) in cultured rat vascular smooth muscle cells (VSMC). The preincubation of cells with the 110 mM extracellular Na+ ([Na+]e) solution supplemented with 30 mM choline chloride for 60 minutes enhanced the effect of AVP- (1 x 10(-8) M) induced VSMC contraction. The treatment of 110 mM [Na+]e solution also enhanced the cellular contractile response to the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate and 1-oleoyl-2-acetyl-glycerol. Furthermore, preincubation with the 110 mM [Na+]e solution also potentiated the effect of 1 x 10(-8) M AVP, but not 1 x 10(-6) M, to increase the cytosolic-free Ca2+ ([Ca2+]i) concentration. The 110 mM [Na+]e media decreased the basal intracellular Na+ concentration and increased intracellular 45Ca2+ accumulation, basal [Ca2+]i and AVP-produced 45Ca2+ efflux. These effects of 110 mM [Na+]e solution to enhance the vascular action of AVP were abolished by using Ca(2+)-free 110 mM [Na+]e solution during the preincubation period. The preincubation with the 110 mM [Na+]e solution did not change either the Kd and Bmax of AVP V1 receptor of VSMC or the AVP-induced production of inositol 1,4,5-trisphosphate. The present in vitro results therefore indicate that the diminished extracellular fluid sodium concentration within a range observed in clinical hyponatremic states enhances the vascular action of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Cellular action and interactions of arginine vasopressin in vascular smooth muscle: mechanisms and clinical implications.

In recent years, much has been learned about the vascular action of arginine vasopressin (AVP) including (1) the structure, internalization, and recycling of the V1 AVP receptor; (2) the AVP postreceptor signaling events for the initial and sustained vascular smooth muscle cell contraction as well as the hormone's mitogenic effect; (3) the process of homologous and heterologous AVP desensitization in vascular smooth muscle cells; (4) the interaction of AVP with other vasoconstrictor and vasodilator hormones; (5) the vascular interaction of AVP with endothelial events; and (6) the vascular interactions that may occur with systemic acidemia or alkalemia as well as with ethanol. The various potential clinical and biochemical implications of these results are discussed briefly.

Animals↗
PubMed1993

[Calciphylaxis in chronic renal failure].

Three cases of calciphylaxis in patients with terminal renal insufficiency are discussed. The existence of metastatic calcifications, mainly vascular, in patients with chronic renal insufficiency is frequent. However calciphylaxis is a process which is rarely found in these patients. This entity is characterized by the obliteration of small vessels with ischemia and necrosis. The exceptionality of the disease, its difficult treatment and poor evolution make calciphylaxis a bad prognostic complication which should be considered in the differential diagnosis of cutaneous lesions in patients with chronic renal insufficiency.

Aged↗
PubMed1992

Aggregation of human polymorphonuclear leukocytes by endothelin: role of platelet-activating factor.

The mechanisms by which endothelin-1 (ET-1) acts on polymorphonuclear leukocytes (PMN) are insufficiently known. In this study, we assessed the hypotheses that ET-1 is a PMN-aggregating agent, and that platelet-activating factor (PAF) is the principal mediator of ET-1-induced PMN aggregation. ET-1 induced dose-related PMN aggregation, which started 1 min after ET-1 exposure. Two different specific PAF receptor antagonists blocked the effect of ET-1 on PMN aggregation. In addition, ET-1 induced a significant increase in the production of PAF by PMN after 2 to 5 min of ET-1 incubation. ET-1 induced PAF release from PMN rather than accumulation. This PAF production was dependent on intra- and extracellular Ca2+. In this regard, the PAF receptor antagonists significantly blunted the ET-1-induced peak in cytosolic free Ca2+ ([Ca2+]i). Our results, therefore, indicate that ET-1 is effective in causing aggregation of human PMN and that its action appears to be mediated by PAF production via a Ca(2+)-dependent mechanism.

Azepines↗
PubMed1992

Effect of recombinant human growth hormone in a postpediatric hemodialysis patient with delayed growth.

We present an 18-year-old patient who has been on renal replacement therapy since the age of 11. He had growth retardation and delayed puberty, with a bone age of 13.6 years. Treatment with human recombinant growth hormone (rhGH) resulted in a clearcut increase in height and lean body mass. We emphasize that rhGH treatment could be tried even at a postpediatric age, provided bone radiology suggests that further growth is possible.

Adolescent↗