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I Hanbauer

Publications and source records attributed to I Hanbauer.

52 records · Page 3Linked to original sources
PubMed1975

ATP, cyclic AMP, and magnesium increase the affinity of rat striatal tyrosine hydroxylase for its cofactor.

Treatment of rat striatal tyrosine hydroxylase [tyrosine 3-monooxygenase; L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating); EC 1.14.16.2] with conditions optimal for protein phosphorylation results in the reduction of the tyrosine hydroxylase Km for the cofactor 6-methyltetrahydropterin from 0.50 mM to 0.16 mM. This reaction is dependent upon ATP, 3':5'-cAMP, and Mg++ and causes a marked decrease in the sensitivity to end-product inhibition. Other brain regions and the adrenal gland show a similar response.

Adenosine Triphosphate↗
PubMed1975

Induction of tyrosine hydroxylase elicited by beta adrenergic receptor agonists in normal and decentralized sympathetic ganglia: role of cyclic 3',5' - adenosine monophosphate.

A subcutaneous injection of an oil suspension of l-epinephrine (270 mumol/kg), dopamine (270 mumol/kg) or l-norepinephrine (270 mumol/kg), when administered with phenoxybenzamine (32 mumol/kg i.p.) to blocl alpha adrenergic effects, increases the cyclic 3', 5'-adenosine monophosphate (cAMP) content in superior cervical ganglia (SCG) of rats. The increase is highest after l-epinephrine and dopamine and is barely detectable after l-norepinephrine; it lasts longer than 2 hours after l-epinephrine, about 30 minutes after dopamine and is fleeting after l-norepinephrine. The duration of the increase in cAMP elicited by l-epinephrine in SCG of rats is dose-related. Furthermore, when the cAMP increase lasts longer than 90 minutes, 48 hours later the tyrosine hydroxylase (TH) activity in SCG is increased. l0Epinephrine (150 mol/kg s.c.) induces TH in decentralized ganglia. One injection of l-isoproterenol (77 mol/kg i.p.) increases cAMP concentrations in intact and decentralized SCG. This increase lasts only 30 minutes and fails to induce TH 48 hours later. However, if the increase of cAMP concentration is prolonged by four successive injections of l-isoproterenol (15 30-minute intervals) the TH activity of intact and decentralized SCG is increased 48 hours later.l-Isoproterenol (four injections of 77 mumol/kg, each) and l-epinephrine (270 mumol/kg) fail to induce TH in the adrenal medulla. dl-Propranolol (125 mumol/kg i.p.) injected 30 minutes before l-isoproterenol blocks the increase of cAMP content and the delayed induction of TH activity in SCG. The elevation of TH activity elicited in SCG by beta adrenergic receptor agonists is always preceded by an increase of cAMP concentration lasting 90 minutes or longer. However, the induction of TH elicited by cold exposure or by reserpine administration can occur without an apparent increase in ganglionic cAMP concentration.

Adrenal Medulla↗
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↗