Gadolinium ions inhibit exocytotic vasopressin release from the rat neurohypophysis.

Abstract

SUMMARY1. Single rat neurointermediate lobes (n.i.l.s) were fixed by their stalks to a platinum wire clip electrode and incubated in oxygenated Krebs-HEPES medium. Vasopressin release into the medium was determined by radioimmunoassay. Vasopressin secretion was increased by different stimuli and the effects of gadolinium (Gd3+) were tested.2. Electrical stimulation (15 Hz, three times 1 min with 1 min intervals) increased vasopressin release in a calcium-dependent manner. Gd3+ (10 ftM to 3 mM) inhibited the evoked release of vasopressin in a concentration-dependent fashion; at 3 mm the inhibition was 980. The inhibitory effect of Gd3+ up to 300 /tM was antagonized by increasing the calcium concentration in the medium up to 6 mm. The effects of 1 and 3 mM-Gd3+ were unaffected by increasing the calcium concentration.3. Exposure of n.i.l.s to depolarizing concentrations of potassium (high K+, 60 mM, 30 min) increased the vasopressin release more than 33-fold. The elevated vasopressin release remained constant during six consecutive 5 min periods. In the initial 5 min period 300 /uM-Gd3+ reduced the evoked vasopressin release by 800 but during the last 5 min period only by 3000. At 3 mM-Gd3+ vasopressin release was completely blocked during the whole time of incubation with high K+.4. Vasopressin release induced by exposure of n.i.l.s to cold (4 TC, 20 min) was completely inhibited by 3 mM-Gd3+, but reduced by only 250% in the presence of 300 /tM-Gd3+.5. Vasopressin release induced by incubation of n.i.l.s with the ionophore X-537A

Changes of quantal transmitter release caused by gadolinium ions at the frog neuromuscular junction

“…The results support the view that Gd3+ blocks N-type Ca2 + channels (Docherty, 1988) and suggest that such channels are the major type involved in nerve-impulse evoked transmitter release from frog motor nerve terminals. These findings agree with previous studies showing that Gd3+ inhibits [3H]-noradrenaline and vasopressin release (Bourne & Trifaro, 1982;Muscholl et al, 1985) and effectively reduced depolarization-induced 45Ca2+ uptake into cultured chromaffin cells and rat brain synaptosomes (Nachshen, 1984).…”

“…On isolated adrenal medullary cells and in the rat neurohypophysis no effect of Gd3+ was detected on the basal release of [3H]-noradrenaline and vasopressin (Bourne & Trifaro, 1982;Muscholl et al, 1985) while in striatal synaptosomal preparations Gd3 + slightly increased basal [3H]-dopamine release (Sheer, 1989). The increase in spontaneous quantal release caused by Gd3+ is most probably the result of its entry into motor nerve terminals and its intracellular action is reminiscent of the action of La3 + (Curtis et al, 1986).…”

Proliferation of Hepatocytes and Attenuation from Carbon Tetrachloride Hepatotoxicity by Gadolinium Chloride in Rats

“…Ogino et al (1994) suggested that zinc hydroxide, a colloidal form of zinc under neutral conditions, was taken up by rat neutrophils, and that it stimulated respiratory burst. Moreover, it is well known that gadolinium ions have various pharmacological actions (Dos Remedios & Barden 1977;Bourne & Trifaro 1982;Muscholl et al 1985;Yang & Sachs 1989;Bear & Li 1991). Based on these findings, we speculated that GdC13 may affect Kupffer cell function.…”

“…Edwards et al (1993) reported that GdC& inhibited CCLinduced liver injury via the inhibition of Kupffer cell functions. However, gadolinium ions have various pharmacological actions such as an inhibition of the polymerization of G-actin to form F-actin (Dos Remedios & Barden 1977), release of catecholamine from isolated adrenal medullary cells (Bourne & Trifaro 1982), and blocking of calcium channels (Bourne & Trifaro 1982;Muscholl et al 1985;Yang & Sachs 1989;Bear & Li 1991).…”

Επιδράσεις του Ευρωπίου (Εu), στην εμβρυοφυσιολογία του Danio rerio

“…Τα ιόντα των λανθανιδών μπορούν να προσδεθούν στην κυτταρική επιφάνεια καταστρέφοντας την σταθερότητα των μεμβρανών και αυξάνοντας την διαπερατότητα τους (Chang, 1991 (Ma et al, 1993). Ως συνέπεια των γεγονότων αυτών είναι η παύση των νευρικών ώσεων και η συστολή των λείων, σκελετικών και καρδιακών μυών, η λειτουργία του ενδοθηλίου των αγγείων και σταματούν τις διάφορες ορμονικές αποκρίσεις (Barry et al, 1978;Morris, 1980;Muscholl et al, 1985).…”