Navegando por Palavras-chave "PARATHYROID HORMONE"

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    EFFECT OF ALUMINUM ON URINARY ACIDIFICATION IN THE RAT - INFLUENCE OF PARATHYROID-HORMONE
    (Portland Press, 1991-10-01) Gil, Frida Zaladek [UNIFESP]; Silva, VLC; Cavanal, Maria de Fátima [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    1. The influence of thyroparathyroidectomy and/or acidosis on renal function and specifically on acid excretion was studied in rats treated with a cumulative dose of 2 mg of aluminium.2. Aluminium-treated and non-treated thyroparathyroidectomized rats showed a significant decrease in glomerular filtration rate and in the urinary/plasma inulin ratio without alteration in net acid excretion.3. Non-treated thyroparathyroidectomized acidotic rats showed a significant fall in the amount of ammonium excreted and in overall acid excretion, suggesting that parathyroid hormone participates in an important way in the defence against metabolic acidosis.4. The effects of acidosis, thyroparathyroidectomy and aluminium treatment on renal function parameters were not additive, suggesting a common final mechanism. In normal or acidotic aluminium-treated rats, thyroparathyroidectomy had no effect on renal acid excretion, suggesting that aluminium even in low doses inhibited the action of PTH on the renal tubule.5. After exposure to aluminium, the relative inhibition of PTH on the renal tubule may become an additional factor that could contribute to the worsening of clinical conditions in which an inappropriate retention of acid loads can occur.
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    EFFECTS OF PARATHYROID-HORMONE AND CALCIUM AND THEIR INTERRELATIONSHIP ON URINARY ACIDIFICATION IN THE RAT
    (Portland Press, 1992-12-01) Gil, Frida Zaladek [UNIFESP]; Silva, VLC; Cavanal, Maria de Fátima [UNIFESP]; Malnic, G.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    1. The influence of thyroparathyroidectomy on renal function and specifically on acid excretion was studied in rats with or without oral supplementation of calcium.2. Thyroparathyroidectomy caused a significant decrease in glomerular filtration rate, in the urinary/plasma inulin ratio and in overall acid excretion. These changes were not corrected by calcium supplementation.3. Rates of proximal tubular acidification were studied by means of double-barrelled resin/reference microelectrodes. Acidification half-time was significantly increased in both thyroparathyroidectomized and calcium-supplemented thyroparathyroidectomized rats (8.38 s and 7.40 s, respectively) compared with control rats (5.44 s).4. When 10(-6) mol/l A23187, a calcium ionophore, was added to the luminal bicarbonate solution, the acidification half-time returned to 3.97 s in the thyroparathyroidectomized rats, whereas no significant changes were detected in the properties of acidification in the control rats.5. These data show that parathyroid hormone and cellular calcium are important factors involved in proximal tubular H+ secretion, which appears to be largely dependent on a well-defined concentration range of these agents.
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    EFFECTS OF PARATHYROID-HORMONE ON URINARY ACIDIFICATION IN THE RAT
    (Assoc Bras Divulg Cientifica, 1991-01-01) Gil, Frida Zaladek [UNIFESP]; Costasilva, V. L.; Malnic, G.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    To evaluate the effects of parathyroid hormone (PTH) on urinary acidification parameters, thyroparathyroidectomy was performed in normal (TPTX) and in calcium-supplemented rats (TPTX+Ca2+). Both groups were supplemented with thyroxin. Glomerular filtration rate (GFR) fell from 7.79 +/- 0.33 in the control group (C) to 4.88 +/- 0.26 ml min-1 kg-1 in TPTX, while net acid excretion fell from 5.65 +/- 0.22 in C to 3.76 +/- 0.25-mu-mol min-1 kg-1 in TPTX. Kinetic data of urinary acidification obtained by microperfusion techniques in proximal tubules showed that the half-time of acidification (t/2) rose from 4.75 +/- 0.24 s in C to 8.97 +/- 0.64 s in TPTX and persisted elevated in TPTX+Ca2+ (7.40 +/- 0.43 s); in the latter group, stationary pH was not significantly different from that of the control group. Bicarbonate reabsorption (J(HCO3)) fell from 2.18 +/- 0.15 in C to 0.823 +/- 0.082 in TPTX and was 1.53 +/- 0.073 nmol s-1 cm-2 in TPTX+Ca2+. These data suggest that normal pH gradients depend on normal calcium levels, but acidification half-times are dependent on PTH, which also contributes to keeping glomerular hemodynamics and acidification rates at normal levels.
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    PARATHYROID-HORMONE SECRETORY RESERVE IN PATIENTS SUBMITTED TO 131-IODINE THERAPY FOR HYPERTHYROIDISM
    (Assoc Bras Divulg Cientifica, 1991-01-01) Vieira, Jose Gilberto Henriques [UNIFESP]; Brandao, Cynthia Maria Alvares [UNIFESP]; Kasamatsu, Teresa Sayoko [UNIFESP]; Furlanetto, Reinaldo Perrone [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Twelve euthyroid patients who had been treated with I-131 for hyperthyroidism due to Graves' disease and six normal controls were submitted to an EDTA infusion test. Ionized calcium and parathyroid hormone were measured in serum samples collected every 10 min during the 2-h test. Basal values for calcium (1.22 +/- 0.03 vs 1.23 +/- 0.03 pmol/l, mean +/- SD, controls vs patients) and parathyroid hormone (3.3 +/- 0.65 vs 5.1 +/- 2.32 pmol/l) as well as maximum response during infusion (1.01 +/- 0.04 vs 1.01 +/- 0.05 for calcium and 12.0 +/- 2.2 vs 13.1 +/- 3.7 for parathyroid hormone) were not significantly different. We conclude that I-131 treatment for hyperthyroidism due to Graves' disease had no effect on the parathyroid gland secretory reserve of the patients studied.