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Biomedical subjects

I Hanbauer

Publications and source records attributed to I Hanbauer.

90 records · Page 5Linked to original sources
PubMed1974

Effects of vinblastine on noradrenergic axons.

1 The effects of vinblastine and 6-hydroxydopamine (6-OHDA) on various parameters of adrenergic neurone functions in the rat were examined and compared.2 During the first 12 h after injection of vinblastine, although the concentration of cardiac noradrenaline was unaltered, the turnover rate of the catecholamine in the heart was reduced to 40 ng g(-1) h(-1) compared to a rate of 66 ng g(-1) h(-1) in the hearts of animals treated with 0.9% w/v NaCl solution.3 The uptake of noradrenaline by rat atria in vitro was inhibited by vinblastine (2.5 x 10(-4) M) or 6-OHDA (5 x 10(-5) M), but only the inhibitory effect of vinblastine was readily reversible. The in vitro uptake of noradrenaline by atria of vinblastine- or 6-OHDA-treated rats was found to be impaired two days after injection of the drugs. After 14 days, however, the noradrenaline uptake was 71% of control values after vinblastine and 91% after 6-OHDA.4 In addition to intensely fluorescent nerve trunks in epicardial connective tissue septa, a decrease in the number of fluorescent adrenergic terminals in the atria and ventricles could be observed two days after vinblastine injection. It is suggested that intravenous vinblastine treatment, like 6-OHDA, results in the destruction of adrenergic nerve terminals.

Animals↗
PubMed1973

Effects of vinblastine on catecholamine-biosynthetic enzymes in heart, sympathetic ganglion and adrenal glands of rats.

1. The effect of vinblastine on the activities of dopamine-beta-hydroxylase (DBH) in heart, superior cervical ganglion and adrenal glands of rats and tyrosine hydroxylase (TH) and phenylethanolamine-N-methyl transferase (PNMT) in adrenal glands was examined.2. In the superior cervical ganglion and heart, DBH activity decreased within hours, reached a minimum in 3 to 5 days and slowly returned towards normal over the next 2 weeks.3. There was an increase in the activities of TH, DBH and PNMT in adrenal glands which was prevented by adrenal denervation.4. When the same total dose of vinblastine was administered subdivided over a period of 5 days, enzyme activities in heart, superior cervical ganglion or adrenal glands remained unchanged.

Adrenal Glands↗
PubMed1972

Axonal sprouts and ( 3 H)norepinephrine uptake by superior cervical ganglia in organ culture.

Superior cervical ganglia from adult rats maintained in organ culture show a progressive increase in the rate of uptake of [(3)H]norepinephrine. The enhanced uptake of norepinephrine is a consequence of the development of axonal sprouts. Formation of axonal sprouts, which appear to have many of the properties of sympathetic nerve endings, is inhibited by colchicine and vinblastine, presumably because of the interaction of these drugs with neurotubular protein.

Animals↗
PubMedDate not supplied

Rat mesencephalic neuronal cells cultured for different periods as a model of dopamine transporter ontogenesis.

Ventral mesencephalic neurons contained only low-affinity and sodium-independent binding sites of [3H]WIN 35,428 (marker of dopamine transporter) during the first 10 d in primary cultures. These sites were present in cytosol, and they are not very probably related to dopamine transporter. After 12 d in culture, membrane-bound, high-affinity, and sodium-dependent [3H]WIN 35,428 binding sites were detected. In membranes prepared from cells 14 d in culture, cocaine displaced [3H]WIN 35,428 binding with similar potency to that in striatal membranes of adult rat brain. The high-affinity [3H]WIN 35,428 binding sites in mesencephalic neuronal cell cultures are very probably related to dopamine transporter. The development of high-affinity [3H]WIN 35,428 binding sites in neurons cultured for different time periods could be a useful model of dopamine transporter ontogenesis.

Animals↗
PubMedDate not supplied

[Met5]-enkephalin-like peptides of the adrenal medulla: release by nerve stimulation and functional implications.

In adrenal chromaffin cells, various molecular forms of polypeptides cross-reacting with [met5]-enkephalin antisera are stored in granules together with catecholamines and soluble proteins. Splanchnic nerve stimulation increases the release of enkephalin-like peptides from the adrenal gland into the adrenal vein. The release of these peptides appears to be mediated by a cholinergic nicotinic receptor. Fractionation of plasma extracts on Bio-gel P-2 shows the presence of only low molecular weight peptides in the resting condition. The low molecular weight fraction contains mainly [met5]-enkephalin and [leu5]-enkephalin. When the splanchnic nerve is stimulated high and low molecular weight peptides are released and the amount of low molecular weight peptides in plasma is increased. The content of enkephalin-like peptides in adrenal venous plasma was similar in control and reserpinized dogs. Splanchnic nerve stimulation increased the peptide content but not the epinephrine content of plasma in reserpinized dogs. This also caused a fall of arterial blood pressure which could be prevented by pretreatment with naloxone. A decrease in blood pressure was also directly elicited by the injection of [met5]-enkephalin-[arg6-phe7]. The duration of the hypotensive effect of this peptide was prolonged by prior injection of captopril.

Adrenal Medulla↗
PubMedDate not supplied

Role of antioxidants in the nitric oxide-elicited inhibition of dopamine uptake in cultured mesencephalic neurons. Insights into potential mechanisms of nitric oxide-mediated neurotoxicity.

Under aerobic conditions the addition of (C2N5)2N(N[O]NO)-.Na+(DEA/NO), S-nitroso-N-acetyl penicillamine and nitric oxide (NO)-saturated buffer, but not S-nitroso-L-glutathione, to dopamine solutions resulted in dopamine o-semiquinone formation that was dependent on the formation of a NO/oxygen intermediate. High pressure liquid chromatography (HPLC) electrochemical analysis of dopamine demonstrated that the DEA/NO-induced oxidation of dopamine was abrogated in the presence of the antioxidants, ascorbate and glutathione. NO spontaneously released from DEA/NO decreased [3H]dopamine accumulation in primary cultures of mesencephalic neurons in a dose-dependent fashion. In contrast, [3H] gamma-aminobutyric acid uptake by mesencephalic neurons tested under the same conditions was unchanged. When DEA/NO was added to incubation buffer that contained [3H]dopamine and the antioxidant, ascorbate or glutathione, [3H]dopamine uptake was also inhibited. These data excluded that oxidation of extracellular [3H]dopamine by the intermediates of the NO/O2 reaction could have caused this decrease. Instead, NO may have acted directly on a not yet identified target operative in the regulation of dopamine storage and release. Analysis of the rate constants for the NO reaction with ascorbate, glutathione and dopamine revealed that dopamine quinone formation was delayed by the presence of antioxidants. Since the formation of NO as well as neurotransmitter release are activated during ischemia reperfusion injury, it is possible that prolonged NO exposure could deplete antioxidants and facilitate the oxidation of dopamine and thereby cause neurotoxicity.

Animals↗
PubMedDate not supplied

Reaction kinetics for nitrosation of cysteine and glutathione in aerobic nitric oxide solutions at neutral pH. Insights into the fate and physiological effects of intermediates generated in the NO/O2 reaction.

The critical regulatory function of nitric oxide (NO) in many physiologic processes is well established. However, in an aerobic aqueous environment NO is known to generate one or more reactive and potentially toxic nitrogen oxide (NOx) metabolites. This has led to the speculation that mechanisms must exist in vivo by which these reactive intermediates are detoxified, although the nature of these mechanisms has yet to be elucidated. This report demonstrates that among the primary bioorganic products of the reaction of cellular constituents with the intermediates of the NO/O2 reaction are S-nitrosothiol (S-NO) adducts. Anaerobic solutions of NO are not capable of nitrosating cysteine or glutathione, while S-NO adducts of these amino acids are readily formed in the presence of O2 and NO. Investigation of the kinetics for the formation of these S-NO adducts has revealed a rate equation of d[RSNO]/dt = kSNO[NO]2[O2], where kSNO = (6 +/- 2) x 10(6) M-2S-1, a value identical to that for the formation of reactive intermediates in the autoxidation of NO. Competition studies performed with a variety of amino acids, glutathione, and azide have shown that cysteine residues have an affinity for the NOx species that is 3 orders of magnitude greater than that of the nonsulfhydryl amino acids, and > 10(6) times greater than that of the exocyclic amino groups of DNA bases. The dipeptide alanyltyrosine reacts with the intermediates of the NO/O2 reaction with an affinity 150 times less than that of the sulfhydryl-containing compounds. Furthermore, Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗