Neuronal and extraneuronal uptake and metabolism of catecholamines

Graefe, Karl Heinz; Henseling, M.

doi:10.1016/0306-3623(83)90058-7

Cited by 59 publications

(29 citation statements)

References 29 publications

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“…Stimulation of perivascular adrenergic nerves releases into the perfusate noradrenaline (NA) and its metabolites 3,4-dihydroxyphenylglycol (DOPEG), 3-methoxy-4-hydroxyphenylglycol (MOPEG), normetanephrine (NM) or 3-methoxy-4-hydroxymandelic acid (VMA) (Graefe & Henseling, 1983). Increased outflow of DOPEG during field stimulation is largely related to NA which had been taken up into the nerve terminal.…”

Section: Introductionmentioning

confidence: 99%

Effects of tyramine on noradrenaline outflow and electrical responses induced by field stimulation in the perfused rabbit ear artery

Miyahara

Suzuki

1985

British J Pharmacology

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In the perfused rabbit ear artery the basal outflows of noradrenaline (NA) and 3,4‐dihydroxyphenylglycol (DOPEG) were < 1 ng g−1 and 1–2 ng g−1 wet weight of tissue respectively. Field stimulation increased outflows of NA and DOPEG in a frequency‐dependent manner, and they reached the maximum value at frequencies over 5 Hz. Tyramine (1 × 10−6 − 1 × 10−4 M) increased basal outflow of NA and DOPEG, in a dose‐dependent manner. This effect was not blocked by tetrodotoxin (TTX, 3 × 10−7 M), but was prevented by pretreatment with 6‐hydroxydopamine (6‐OHDA). Tyramine increased the field stimulation‐induced outflow of NA but not that of DOPEG in a dose‐dependent manner. Cocaine (1 × 10−5 M) reduced the increased outflow of NA induced by tyramine at rest and during field stimulation, without modifying DOPEG‐outflow. Guanethidine (5 × 10−6 M), increased outflows of NA and DOPEG at rest, and reduced the NA outflow induced by field stimulation. Pretreatment with guanethidine (5 × 10−6 M) did not block the action of tyramine on NA and DOPEG basal outflows. Additional application of guanethidine during the presence of tyramine did reduce the outflow of NA induced by field stimulation, but did not modify the outflow of NA and DOPEG at rest. Tyramine at concentrations over 1 × 10−5 M depolarized the smooth muscle membrane of the rabbit ear artery. After chemical denervation with 6‐hydroxydopamine (6‐OHDA) the depolarizing action of tyramine was reduced. Tyramine‐induced depolarization was attenuated by prazosin (5 × 10−6 M) or phentolamine (5 × 10−6 M), but not by guanethidine (5 × 10−6 M). In 6‐OHDA‐denervated tissues, tyramine‐induced depolarization was attenuated by phentolamine but not by prazosin. Field stimulation evoked excitatory junction potential (e.j.p.), slow depolarization and spike potential in the rabbit ear artery. Tyramine reduced, while guanethidine blocked these electrical responses. Tyramine did not alter the facilitation process of e.j.ps. In tissues pretreated with guanethidine, tyramine evoked either no electrical response or a slow depolarization during field stimulation. The slow depolarization was blocked by prazosin. Tyramine reduced the NA content of tissues in a dose‐dependent manner (by 31% at 10−4 M). Guanethidine (5 × 10−6 M) reduced the NA content by 20%. We conclude that in the rabbit ear artery, tyramine depolarizes the smooth muscle membrane indirectly by releasing neuronal NA which acts on α‐adrenoceptors, and directly by an action on the smooth muscle cells. Two NA compartments (guanethidine‐sensitive and tyramine‐sensitive NA) could be identified. Field stimulation releases the former with associated generation of e.j.p. and slow depolarization whilst the release of the latter is not accompanied by e.j.p. generation.

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Section: Introductionmentioning

confidence: 99%

Effects of tyramine on noradrenaline outflow and electrical responses induced by field stimulation in the perfused rabbit ear artery

Miyahara

Suzuki

1985

British J Pharmacology

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“…Furthermore, VMAT-2 has higher affinity for NA than MAO, which implies that over 70% of the recaptured NA through NET is sequestered into storage vesicles before being metabolized (Bloom, 2006). Therefore, under normal physiological conditions, the inhibition of MAO has little effect Trendelenburg, 1970, Graefe andHenseling, 1983). Rather than impairing the catecholamine uptake, short-term inhibition of intraneuronal MAO leads to higher retention of recaptured transmitter by VMAT-2 and, thus, an apparent increase in the net uptake of the transmitter (Furchgott and Garcia, 1968).…”

Section: The Cross-talk Between Catecholamine Catabolic Enzymes and Tmentioning

confidence: 99%

“…In both neuronal and extraneuronal metabolizing systems, the inactivation of catecholamines occurs in a coordinated fashion, with uptake being followed by metabolism (Graefe and Henseling, 1983). Most of the metabolism of catecholamines takes place in the same cells where they are produced, even before their exocytotic release (Figure 4).…”

Section: The Metabolites Of Catecholaminesmentioning

confidence: 99%

Adrenaline and Noradrenaline: Partners and Actors in the Same Play"

Costa¹,

Carvalho²,

Bastos³

et al. 2012

Neuroscience - Dealing With Frontiers

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“…This means that most of the norepinephrine produced and released by nerves is metabolized within the nerves themselves (Figure 2). Because monoamine oxidase (MAO) is the only catecholamine-metabolizing enzyme present in sympathetic nerves, the norepinephrine metabolized within these nerves is all converted to dihydroxyphenylglycol (DHPG) (11)(12)(13). As a consequence, the DHPG appearing in Figure 2 -Quantitative diagram showing neuronal and extraneuronal pathways of norepinephrine (NE) metabolism before and after entry into the bloodstream.…”

Section: Disposition Of Catecholamines Derived From the Sympatho-adrementioning

confidence: 99%

“…plasma is almost exclusively produced in sympathetic nerves, whereas the additional presence of catechol-O-methyltransferase in extraneuronal cells means that normetanephrine is exclusively produced from norepinephrine in extraneuronal cells, such as smooth muscle cells or liver cells (9,11). Much of the DHPG formed in nerves is metabolized further to 3-methoxy-4-hydroxyphenylglycol (MHPG) by catechol-O-methyltransferase in extraneuronal cells (14).…”

Section: Disposition Of Catecholamines Derived From the Sympatho-adrementioning

confidence: 99%

Plasma metanephrines: a novel and cost-effective test for pheochromocytoma

Eisenhofer

Walther

Keiser

et al. 2000

Braz J Med Biol Res

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Pheochromocytomas are rare chromaffin cell tumors that nevertheless must be excluded in large numbers of patients who develop sustained or episodic hypertension as well as in many others with suggestive symptoms or with a familial history of pheochromocytoma. Diagnosis of pheochromocytoma depends importantly on biochemical evidence of excess catecholamine production by a tumor. Imperfect sensitivity and specificity of commonly available biochemical tests and the low incidence of the tumor among the tested population mean that considerable time and effort can be expended in confirming or ruling out pheochromocytoma in patients where the tumor is suspected. Measurements of plasma free metanephrines provide a superior test compared to other available tests for diagnosis of pheochromocytoma. In particular, the high sensitivity of plasma free metanephrines means that a normal test result reliably excludes all but the smallest of pheochromocytomas so that no other tests are necessary. Measurements of plasma free metanephrines, when systematically combined with other diagnostic procedures outlined in this review, provide a more efficient, reliable and cost-effective approach for diagnosis of pheochromocytoma than offered by previously available approaches.

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Neuronal and extraneuronal uptake and metabolism of catecholamines

Cited by 59 publications

References 29 publications

Effects of tyramine on noradrenaline outflow and electrical responses induced by field stimulation in the perfused rabbit ear artery

Effects of tyramine on noradrenaline outflow and electrical responses induced by field stimulation in the perfused rabbit ear artery

Adrenaline and Noradrenaline: Partners and Actors in the Same Play"

Plasma metanephrines: a novel and cost-effective test for pheochromocytoma

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