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1.
Summary— The regulation and role of the intracellular Ca2+ pools were studied in rat peritoneal mast cells. Cytosolic free calcium concentration ([Ca2+ ]i) was monitored in fura-2 loaded mast cells. In the presence of Ca2+ and K+, compound 48/80 induced a biphasic increase in [Ca2+ ]i composed of a fast transient phase and an apparent sustained phase. The sustained phase was partially inhibited by the addition of Mn2+ . DTPA, a cell-impermeant chelator of Mn2+ , reversed this inhibition, suggesting that a quenching of fura-2 fluorescence occurs in the extracellular medium. In the absence of extracellular Ca2+ , the transient phase, but not the sustained one, could be preserved, provided that mast cells were depolarized. The transient phase was completely abolished by thapsigargin, a microsomal Ca2+ -ATPase inhibitor. Maximum histamine release induced by either compound 48/80 or antigen was obtained in the absence of added Ca2+ only when mast cells were depolarized. These histamine releases were inhibited by low doses (< 30 nM) of thapsigargin. Thapsigargin at higher doses induced histamine release which was unaffected by changing the plasma membrane potential, but was completely dependent on extracellular Ca2+ , showing that a Ca2+ influx is required for thapsigargin-induced exocytosis. Together, these results suggest that the mobilization of Ca2+ from thapsigargin sensitive-intracellular pools induced by compound 48/80 or antigen is sufficient to trigger histamine release. The modulation of these pools by the plasma membrane potential suggest their localization is close to the plasma membrane. 相似文献
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Bals-Pratsch M; De Geyter C; Muller T; Frieling U; Lerchl A; Pirke KM; Hanker JP; Becker-Carus C; Nieschlag E 《Human reproduction (Oxford, England)》1997,12(5):896-904
Preliminary data have suggested that female infertility due to corpus
luteum insufficiency may be caused by subclinical hypothyroidism
[exaggerated thyroid-stimulating hormone (TSH) response to thyrotrophin-
releasing hormone (TRH) stimulation]. L-Thyroxine supplementation has been
recommended to achieve pregnancies in subclinical hypothyroid women. This
controlled study was carried out in order to investigate the biochemical
diagnosis of subclinical hypothyroidism as a possible infertility factor.
Five infertile patients (aged 25-36 years) with subclinical hypothyroidism
(n = 4, stimulated TSH >20 microU/ml) or primary hypothyroidism (n = 1)
and five healthy controls (aged 22-39 years) with normal thyroid function
(stimulated TSH <15 microU/ml), regular cycles and no history of
infertility were studied in the early follicular phase. In the pre-study
evaluation, eight of 23 volunteers (34.8%) had to be excluded because of
subclinical hypothyroidism with stimulated TSH values (TSHs) >15
microU/ml. Cycle function of patients and controls was compared by the
method of LH pulse pattern analysis. Therefore blood samples were drawn
every 10 min during a 24 h period. Sleep was recorded from midnight to 7
a.m. Repetition of the TRH tests at the end of the 24 h blood sampling
period confirmed the difference in stimulated TSH values of the two study
groups. Pulse analysis for luteinizing hormone (LH), TSH and prolactin
showed no differences between patients and controls for pulse frequency,
amplitude, height, length, area under curve (AUC) and the 24 h mean. Even
the hypothyroid patient had a normal LH pulse pattern. Additional
measurement of melatonin in pooled sera every 30 min gave the
well-documented diurnal profiles during day and night for both groups.
Patients had significantly higher melatonin values at seven time points
during the night. Peaks for LH, TSH, prolactin and cortisol were correlated
with the sleep stages wake, rapid eye movement, 1 + 2 and 3 + 4. We
concluded that corpus luteum insufficiency in female infertility cannot be
explained by subclinical hypothyroidism and thus should not be treated with
L-thyroxine for fertility reasons.
相似文献
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