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Biomedical subjects

I Hanbauer

Publications and source records attributed to I Hanbauer.

At least 37 records · Page 2Linked to original sources
PubMed1985

Evidence for down-regulation of 3H-nitrendipine recognition sites in mouse brain after long-term treatment with nifedipine or verapamil.

Mice were fed powdered food which contained nifedipine, verapamil or diltiazem for 28 days. Long lasting treatment with nifedipine (0.28 mg/g b.w./day) or verapamil (0.27 mg/g b.w./day), but not with diltiazem (0.38 mg/g b.w./day) reduced the number of 3H-nitrendipine recognition sites in membranes prepared from cerebral cortex, caudate nucleus, and hippocampus. In addition, the veratridine-elicited stimulation of 45Ca-uptake in slices of the same brain areas was decreased in mice which were fed nifedipine or verapamil for 28 days.

Animals↗
PubMed1985

Dopamine uptake is differentially regulated in rat striatum and nucleus accumbens.

Active uptake of 3,4-dihydroxyphenylethylamine (dopamine) is sodium- and temperature-dependent, strongly inhibited by benztropine and nomifensine, and present in corpus striatum and nucleus accumbens. In rat striatum dopamine uptake is related to a receptor that is specifically labelled by [3H]cocaine in the presence of Na+ and is located on dopaminergic terminals. The dopamine uptake is differentially affected in the two areas by single or repeated injections of cocaine. Cocaine inhibits dopamine uptake in slices of corpus striatum. Moreover Na+-dependent [3H]cocaine binding is not detectable in nucleus accumbens. Nomifensine inhibits [3H]dopamine uptake by interacting with low- and high-affinity sites in corpus striatum, but shows only low affinity for dopamine uptake in nucleus accumbens. The present data indicate that different mechanisms are involved in the regulation of dopamine uptake in corpus striatum and nucleus accumbens.

Animals↗
PubMed1978

Heat-stable low molecular weight form of phosphodiesterases from bovine pineal gland.

The 105,000 X g supernatant fraction of bovine pineal gland contains a phosphodiesterase activity that hydrolyzes both cyclic AMP and cyclic GMP. The rate of hydrolysis is 4-5 times greater with cyclic GMP as substrate than with cyclic AMP. Chromatography of supernatant fraction on Sephadex G-150 resolves phosphodiesterase activity into two fractions designated PDE I and PDE II. These are distinguishable on the basis of their molecular size, substrate specificity, and kinetic parameters. PDE I hydrolyzes cyclic GMP at a faster rate than cyclic AMP and has a molecular weight of 163,000. PDE II appears to be a smaller protein with a molecular weight of 24,400 and is specific for cyclic AMP. PDE I has apparent Km values of 83 and 53 micron for cyclic AMP and cyclic GMP, respectively, whereas PDE II exhibits an apparent Km value of 330 micron for cyclic AMP. With subsaturating concentrations of cyclic AMP as substrate, the phosphodiesterase activity of PDE I is inhibited by the addition of cyclic GMP. However, PDE II activity remains unaffected by cyclic GMP even at concentrations up to 125 micron. PDE II appears to be thermostable, losing only 20% of its activity on heating at 80 degrees for 2 min. Similar treatment completely abolishes the enzyme activity of PDE I.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

The regulation of dopamine and noradrenaline in the rat carotid body and its modification by denervation and by hypoxia.

1. The mechanism whereby hypoxia lasting 20 min elicits a decrease in the dopamine content of rat carotid bodies was studied. 2. The concentrations of dopamine, noradrenaline, dihydroxyphenylacetic acid and homovanillic acid in carotid body were measured by a mass-fragmentographic procedure. The turnover rate of dopamine was determined by measuring the elimination rate of dihydroxyphenylacetic acid immediately after inhibition of monoamine oxidase by injection of pargyline. The turnover rate of noradrenaline was derived from measurements of the rate of decline of noradrenaline content after injection of L-methyl-p-tyrosine. 3. The results indicate that hypoxia increases the rate of dopamine release without changing its turnover rate thereby accounting for the decrease in dopamine content. The content and turnover rate of noradrenaline remained unchanged during exposure to hypoxia. 4. Neither the carotid sinus nerve nor the sympathetic innervation appeared to participate in the regulation of dopamine content or turnover rate in carotid bodies of rats either before or during hypoxia. 5. Since transection of the carotid sinus nerve or/and ganglionectomy failed to prevent the decrease of dopamine content caused by hypoxia, it is inferred that low arterial PO2 depletes dopamine stores independently of the above mentioned innervation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Long-term regulatory mechanisms for tyrosine hydroxylase in sympathetic ganglia and carotid body.

The delayed activation of TH elicited by hypoxia in carotid body indirectly suggests that the release of dopamine is part of the responses elicited by hypoxia. The TH activation appears to be independent from nicotinic receptor stimulation and can be abolished by dopaminergic receptor stimulation. Dexamethasone also increases the activity of TH. Since both hypoxia and dexamethasone fail to change the kinetic constants, the long-term increase of TH could be viewed as an expression of new synthesis of enzyme molecules. This assumption is supported by the evidence presented on the prompt kinetic change in PDE, which according to the model proposed by Uzunov et al. (42) expresses the participation of a prompt and sustained response of the second messenger in postsynaptic cells. It remains to be ascertained whether the change in the catalytic activity of PDE which metabolizes the second messenger can be suppressed by dopamine-receptor blockers. Immediate changes of PDE coupled with the delayed increase in TH activity may contribute to a better understanding of the neuronal mechanisms controlling the chemoreceptor function. It is hoped that the continuation of these studies will help to define the function of type I cells in the carotid body.

Adrenal Medulla↗
PubMed1975

Further evidence for a cAMP dependent regulation of tyrosine-3-monoxygenase induction in adrenal medulla: effect of denervation.

Unilateral adrenal denervation caused a gradual decrease of adenylate cyclase activity in rat adrenal medulla. The extent of the increase in adrenal medullary 3',5'-cyclic adenosine monophosphate (cAMP) content elicited by injections of carbamylcholine declined gradually folling adrenal denervation. Three or nine days after denervation carbamylcholine caused rise of cAMP and a delayed increase of tyrosine-3-mono-oxygenase (TH) activity of similar magnitude in intact and denervated adrenal medullae. However, after an interval of 15 days or longer following denervation the increase in TH activity elicited by carbamylcholine was greatly reduced. These results support previous proposals that cAMP is involved as a second messenger in the trans-synaptic induction of TH.

Adenylyl Cyclases↗