Proceedings: The importance of the presynaptic alpha-adrenergic regulation of noradrenaline release from vascular nerves in vivo.
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A geometrical model of inhibition of neuroeffector transmission of the sympathetic system was constructed on the basis of the polymetric method of registration of a complex of somatovegetative indices and multiparametric description of the effect of alpha- and beta-adrenergic blocking agents and adrenomimetic drugs in experiments on intact rats. Similar multiparametric description of the effect of therapeutic doses of adrenergic blocking agents on patients with hypertension was conducted in the clinic. The results obtained in the clinic were interpreted on the basis of the experimental models. The authors show the possibilities of the polymetric method in more scrupulous study of the functional condition of the various links of the vegetative nervous system and in a stricter individual approach to treatment with adrenergic agents.
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Electrical stimulation of the rat sinus nerve altered fluorescence of restored pyridin nucleotides and oxidative flavoproteids in the carotid body cells due to enhancement of cellular respiration. This was followed by an increase of cGMP content in the carotid body. The greatest shifts of these parameters occurred in square-wave stimulation with 20/sec frequency. The effector influences on the carotid body metabolism are most effectively blocked with pentamine and seem to be of cholinergic nature, the transmitter effect of acetylcholine being modulated with enkephalins. The cGMP system may serve as an intermediary of the effector influences.
In the rat isolated vas deferens, exogenous noradrenaline (NA) in concentrations of 5 X 10(-7)-5 X 10(-6) M acting for 10-15 min produced an increase whereas in concentrations above 10(-5) M it produced a decrease of the response to transmural stimulation: the increase being due to raising of the level of its secretion produced by accumulation of NA in nerve endings as well as to augmentation of postsynaptic response to NA resulting from a decrease in its reversal neuronal uptake. The decrease in the organ response to stimulation under the effect of NA at concentrations above 1 X 10(-5) M is due to desensitization of postsynaptic alpha-adrenoceptors.
Cholinergic synaptosomes from electroplax of the ray Ommata discopyge release both ATP and ACh when depolarized with high K+ concentration in the presence of Ca2+. Others have shown that the ATP and ACh are released in the molar ratio found in isolated synaptic vesicles. Thus, it is assumed that the release of ATP reflects exocytosis of synaptic vesicles, and that transmitter release can be indirectly monitored by assaying ATP release. We present further evidence for this assumption and examine the effects of presynaptic neurotoxins on this ATP release. As expected for transmitter release, we find that depolarization-evoked ATP release is supported by Sr2+ and Ba2+ and is inhibited by the Ca channel antagonists Co2+ and Mn2+. Likewise, the presynaptic toxins omega-CmTX and omega-CgTX, omega peptides from the venom of the marine snails Conus magus and Conus geographus, respectively, inhibit 80% of the depolarization-evoked ATP release. Half-maximal inhibition of ATP release occurs with approximately 0.5 microM of either toxin. The toxins' effects are reversible, and when toxin is washed away, the time dependence of recovery of release is approximately first order and half complete within 40 min with omega-CmTX and 15 min with omega-CgTX. The Ca2+ ionophore A23187 induces Ca2+-dependent ATP release from resting synaptosomes. As would be expected of a Ca channel antagonist, omega-CmTX does not affect this ionophore-induced release. Leptinotarsin-d (LPTd), a putative Ca channel agonist from the Colorado potato beetle, evokes Ca2+-dependent ATP release from resting synaptosomes. omega-CmTX does not block LPTd-evoked release of ATP, which suggests that omega-CmTX and LPTd act at different sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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The release of corrosion products during long-term immersion in vitro of dental alloys, with particular reference to dissimilar alloys in contact has been studied. The effects of Hg2+ and Cu2+ in low concentrations on the guinea-pig ileum have also been studied. The following conclusions were drawn: In an aggressive solution the release of elements from amalgams could be continuous and subsurface corrosion could cause a considerable increase in the corrosion products released. The change in microstructure observed in cross-sections of the corroded specimens was related to the amounts of corrosion products released into the saline solution. In an aggressive solution the corrosion products could increase when amalgams, Co-Cr, and Ni-Cr alloys are in contact with gold alloys, a high-Cu amalgam is in contact with a conventional amalgam, a type III gold alloy is in contact with gold alloys for metallo-ceramic purposes. The high-Cu amalgams released more corrosion products into the saline solution than a conventional one. Greater quantities of corrosion products were released from amalgams at pH 4 than at pH 6. Hg2+ and Cu2+ both had diverse and dose-dependent effects on the guinea-pig ileum. In low concentrations, 10nM, both ions exerted effects, probably on the muscle cell membrane.
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