Browsing by Author "Chacón, C"

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    Effect of ammonium chloride and dietary phosphorus in the azotaemic rat.: I.: Renal function and biochemical changes
    (2004) Jara, A; Chacón, C; Ibaceta, M; Valdivieso, A; Felsenfeld, AJ
    Background. Both dietary phosphorus restriction and the ingestion of ammonium chloride (NH4Cl) given to rats on a high-phosphorus diet have been shown to preserve renal function in the azotaemic rat. Parathyroidectomy also has been reported to preserve renal function and, in addition, to prevent kidney hypertrophy in the remnant kidney model. Our goals were (i) to evaluate in azotaemic rats the effect of dietary phosphorus on renal function in a shorter time frame than previously studied and (ii) to determine whether NH4Cl administration (a) enhances the renoprotective effect of dietary phosphorus restriction and (b) improves renal function in the absence of parathyroid hormone (PTH).
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    Effect of ammonium chloride and dietary phosphorus in the azotaemic rat.: Part II -: kidney hypertrophy and calcium deposition
    (2004) Jara, A; Chacón, C; Ibaceta, M; Valdivieso, A; Felsenfeld, AJ
    Background. Kidney hypertrophy is stimulated by both partial nephrectomy and NH4Cl administration. Also, parathyroidectomy (PTX) has been reported to prevent kidney hypertrophy induced by a high protein diet. Our goal was to determine in the azotaemic rat: (i) the combined effects of NH4Cl administration and dietary phosphorus on the development of kidney hypertrophy and calcium deposition in the kidney and (11) whether the absence of parathyroid hormone (PTH) affected the development of kidney hypertrophy and calcium deposition.
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    Effect of calcitriol treatment and withdrawal on hyperparathyroidism in haemodialysis patients with hypocalcaemia
    (2001) Jara, A; Chacón, C; Valdivieso, A; Aris, L; Jalil, R; Felsenfeld, AJ
    Background. Calcitriol is used to treat secondary hyperparathyroidism in dialysis patients. For similarly elevated parathyroid hormone (PTH) levels, the PTH response to calcitriol treatment is believed to he better in hypocalcaemic dialysis patients than in dialysis patients with higher serum calcium values. Furthermore, few studies have evaluated the rapidity of the rebound in serum PTH values after prolonged treatment with calcitriol. Our goal was to evaluate (i) the PTH response to calcitriol treatment in hypocalcaemic haemodialysis patients, (ii) the rapidity of rebound in PTH after calcitriol treatment was stopped, and (iii) whether the effect of calcitriol treatment on PTH levels could be separated from those produced by changes in serum calcium and phosphate values.
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    Failure of high doses of calcitriol and hypercalcaemia to induce apoptosis in hyperplastic parathyroid glands of azotaemic rats
    (2001) Jara, A; González, S; Felsenfeld, AJ; Chacón, C; Valdivieso, A; Jalil, R; Chuaqui, B
    Background. Whether calcitriol administration, which is used to treat secondary hyperparathyroidism in dialysis patients, induces regression of parathyroid-gland hyperplasia remains a subject of interest and debate. If regression of the parathyroid gland were to occur, the presumed mechanism would be apoptosis. However, information on whether high doses of calcitriol can induce apoptosis of parathyroid cells in hyperplastic parathyroid glands is lacking. Consequently, high doses of calcitriol were given to azotaemic rats and the parathyroid glands were evaluated for apoptosis.
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    How dietary phosphate, renal failure and calcitriol administration affect the serum calcium-phosphate relationship in the rat
    (2002) Jara, A; Chacón, C; Felsenfeld, AJ
    Background. The effect of hyperphosphataemia on serum calcium regulation in renal failure has not been well Studied in a setting in which hypercalcaemia is not parathyroid hormone (PTH) mediated. In azotemic rats with a normal serum calcium concentration, in increased dietary phosphate burden affects serum calcium regulation because of its effects on skeletal resistance to PTH, calcitriol production, and possibly intestinal calcium absorption. Our goal was to determine how hyperphosphataemia affected the development of hypercalcaemia during calcitriol-induced hypercalcaemia and PTH suppression in azotemic rats with established hyperparathyroidism.
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    Hyperphosphatemia modestly retards parathyroid hormone suppression during calcitriol-induced hypercalcemia in normal and azotemic rats
    (2002) Jara, A; Chacón, C; Felsenfeld, AJ
    Background/Aims: In in vitro studies, a high phosphate concentration has been shown to directly stimulate parathyroid hormone (PTH) secretion in a normal calcium concentration and to reduce PTH suppression in a high calcium concentration. In hemodialysis patients during dialysis-induced hypercalcemia, the effect of hyperphosphatemia on PTH secretion was less than in vitro studies. Our goal was to determine whether hyperphosphatemia retards PTH suppression during calcitriol-induced hypercalcemia in azotemic rats with hyperparathyroidism. Methods: Rats underwent a two-stage 5/6 nephrectomy or sham operations. After surgery, rats received a high phosphate diet (P 1.2%, Ca 0.6%) for 4 weeks to induce hyperparathyroidism and then were placed on a normal diet (P 0.6%, Ca 0.6%) for two additional weeks to normalize serum calcium values in azotemic rats. At week 7, rats were divided into five groups and before sacrifice received at 24-hour intervals, three doses of calcitriol (CTR) or its vehicle. The five groups and dietary phosphate content were: group 1 - normal renal function (NRF) + 0.6% P + vehicle; group 2 - NRF + 0.6% P + CTR; group 3 - renal failure (RF) + 0.6% P + vehicle; group 4 RF + 1.2% P + CTR; and group 5 - RF + 0.6% P + CTR. Results: In the two CTR-treated groups with marked hypercalcemia (groups 2 and 5), 15.52 +/- 0.26 and 15.12 +/- 0.13 mg/dl, respectively, stepwise regression showed that hyperphosphatemia retarded PTH suppression. When the two azotemic groups treated with CTR (groups 4 and 5) were combined to expand the range of serum calcium values, stepwise regression showed that hypercalcemia suppressed and hyperphosphatemia modestly retarded PTH suppression. Similarly, in groups 4 and 5 combined, correlations were present between PTH and both serum calcium (r = -0.70, p < 0.001) and serum phosphate (r = 0.64, p = 0.001). Conclusions: Hypercalcemia and high doses of calcitriol markedly reduced PTH secretion in azotemic rats despite severe hyperphosphatemia. Even though hyperphosphatemia did retard PTH suppression during hypercalcemia, its effect was small. Copyright (C) 2002 S. Karger AG, Basel.
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    Reduced natriuresis after oral sodium load in cholestatic rats
    (2000) Casar, JC; Valdivieso, A; Bravo, JA; Chacón, C; Boric, MP
    The purpose of this study was to assess the participation of the atrial natriuretic peptide (ANP)-cGMP system in electrolyte and volume handling of cholestatic rats submitted to an acute oral sodium load. Cholestasis was induced by ligation and section of the common bile duct (n = 51), Control rats were sham operated (n = 56), Three weeks after surgery, 24-hr urinary volume, sodium, potassium, cGMP and creatinine excretion were measured. Three days later, animals received 10 mmol/kg NaCl (1 M) by gavage, and urinary excretion was measured for 6 hr. In parallel groups of rats, plasma volume, electrolytes and ANP concentration, extracellular fluid volume (ECFV), and renal medullary ANP-induced cGMP production were determined in basal conditions or 1 hr after oral sodium overload. As compared with controls, cholestatic rats had a larger ECFV and higher plasma ANP (67.2 +/- 5.2 vs 39.7 +/- 3.5 pg/ml), but lower hematocrit and blood volume, and were hyponatremic, Cholestatic rats showed higher basal excretion of sodium, potassium, and volume than controls, but equal urinary cGMP, After the NaCl overload, cholestatic rats showed a reduced sodium excretion but equal urinary cGMP, One hr after sodium overload, both groups showed hypernatremia, but whereas in control rats ECFV and ANP increased (50.7 +/- 4.7 pg/ml), in cholestatic rats ECFV was unchanged, and plasma volume and ANP were reduced (37.5 +/- 5.8 pg/ml), ANP-induced cGMP production in renal medulla was similar in cholestatic and control nonloaded rats (14.2 +/- 5.2 vs 13.4 +/- 2.6 fmol/min/mg), One hr after the load, medullary cGMP production rose significantly in both groups, without difference between them (20.6 +/- 3.1 vs 22.7 +/- 1.7 fmol/min/mg). We conclude that the blunted excretion of an acute oral sodium load in cholestatic rats is associated with lower plasma ANP due to differences in body fluid distribution and cannot be explained by renal refractoriness to ANP.
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    Tissue kallikrein and bradykinin B2 receptor in human uterus in luteal phase and in early and late gestation
    (2001) Valdés, G; Germain, AM; Corthorn, J; Chacón, C; Figueroa, CD; Müller-Esterl, W
    This study was addressed to evaluate the temporo-spatial pattern of key components of the kallikrein-kinin system in human uterus in luteal phase (n = 7), early pregnancy (isolated spontaneous abortions, n = 11; ectopic pregnancies, n = 9), idiopathic preterm deliveries (n = 5), and term gestations (n = 12). Tissue kallikrein mRNA and protein and the type 2 bradykinin receptor (B2R) protein were expressed in luminal and glandular epithelium and in endothelial cells of stromal and myometrial blood vessels, while tissue kallikrein mRNA and B2R, but not tissue kallikrein protein, were observed in decidual cells and in arteriolar and myometrial muscle. A greater signal intensity for tissue kallikrein mRNA and protein and of B2R protein was observed in the early pregnancy samples. The sites and variations of the tissue kallikrein mRNA and protein and of the B2R protein in the human uterus and in fallopian tubes during the luteal phase and in pregnancy coincide with those described for other vasoactive effectors such as nitric oxide, prostacyclins, growth factors, and renin. The uterine localization of the main enzyme and receptor of the tissue kallikrein-kinin system in key sites for embryo attachment, implantation, placentation, maintenance of placental blood flow, and parturition supports the notion that the kallikrein-kinin system participates in these processes, probably through vasodilation, increased vasopermeability, enhanced matrix degradation, stimulation of cell proliferation, and myometrial contractility.
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    Tissue kallikrein in human placenta in early and late gestation
    (2001) Valdés, G; Chacón, C; Corthorn, J; Figueroa, CD; Germain, AM
    This study was addressed to identify kallikrein mRNA and protein in early, preterm, and term human placenta and to evaluate their temporospatial pattern. Kallikrein mRNA was expressed in syncytio/cytotrophoblasts and in the endothelial cells of the floating villi, with a greater intensity in early samples (isolated spontaneous abortions and ectopic pregnancies). Cytotrophoblasts at the base of the anchoring villi, maternal decidua and decidual arteries, endothelial cells of chorionic and basal plate blood vessels, and the amniotic epithelium presented a positive signal. Tissue kallikrein was predominantly observed in syncytiotrophoblasts and had a greater immunoreactivity in first-trimester samples. Intraarterial trophoblasts, blood vessels of the floating villi, basal and chorionic plates, and the amniotic epithelium showed positive immunoreactivity. The sites and variations of the tissue kallikrein mRNA and protein in the human placenta, in different stages of pregnancy, support the hypothesis that this enzyme may participate in the establishment and maintenance of placental blood flow through vasodilation, platelet antiaggregation, cell proliferation, and trophoblast invasion.