The specific activity of retained and released norepinephrine in dog saphenous vein prelabeled with radiolabeled norepinephrine

Rorie, Duane K.; Muldoon, Sheila M.; Tyce, Gertrude M.

doi:10.1016/0024-3205(80)90260-x

Cited by 21 publications

(5 citation statements)

References 19 publications

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“…The differences in specific activity of transmitter at rest and during field stimulation suggest non-uniform labelling of the different 'pools' of noradrenaline in the tissue. The effect was similar whether labelling was done with 3H-noradrenaline or 3H-dopamine and is in agreement with the concept that, noradrenaline that is taken up or newly synthesized is released preferentially during stimulation (Rorie et al, 1980). These results are consistent with the observations that noradrenaline newly synthesized from tyrosine is preferentially released during nerve stimulation (Kopin, Breese, Krauss & Weise, 1968 (Table 3).…”

Section: Discussionsupporting

confidence: 89%

“…However, the specific activity of the noradrenaline released on nerve stimulation was much higher (1.03 Ci mmol-1). This is in agreement with earlier findings that noradrenaline subject to neuronal uptake is preferentially released (Rorie et al, 1980). In addition this neuronal pool is not tracer labelled since at 1.03 Cimmol-1, 32% of NA is due to the labelling procedure.…”

Section: Specific Activities Of Tissue and Released Noradrenalinesupporting

confidence: 93%

“…During this stimulation period efflux was collected. The observed tissue content and overall specific activity of [3H]-noradrenaline ( [3H]-NA) are in agreement with those previously found in the heart and other tissue (Langer, 1970;Farnebo & Malmfors, 1971;Rorie, Muldoon & Tyce, 1980) and indicate that trace labelling of tissue noradrenaline had been accomplished (Table 1). However, the specific activity of the noradrenaline released on nerve stimulation was much higher (1.03 Ci mmol-1).…”

Section: Specific Activities Of Tissue and Released Noradrenalinesupporting

confidence: 87%

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Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Angus¹,

Bobik²,

Jackman³

et al. 1984

British J Pharmacology

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1 Guinea-pig right atria were labelled with [3H]-noradrenaline or [3H1-dopamine before superfusion in a flow-cell. Choice of label did not significantly alter either the relationship between 3H-efflux and number of electrical field pulses or the inhomogeneity of labelling. 2 The relationship between 3H-efflux and frequency of 4 field pulses (0.125 -2 Hz) was hyperbolic and similar to the tachycardia-frequency relationship measured simultaneously. No evidence was found for a U shaped 3H-efflux-frequency relationship (Story, McCulloch, Rand & Standford-Starr, 1981). 3 Phentolamine (1 JiM) did not alter the 3H-efflux or atrial rate responses to 4 field pulses at stimulus levels that gave 50-60% of the maximum rate response. 4 In the presence of neuronal uptake inhibition (desipramine, DMI0.1 gsM), rate and 3H-efflux responses to 4 field pulses were enhanced at all frequencies and were further increased by phentolamine. 5 In the absence of DMI, prolonged trains of field pulses (8 and 12 pulses) at low frequency (0.25 Hz) were not sufficient to activate auto-inhibitory feed-back. At 2 Hz phentolamine enhanced both 3H-efflux and rate responses at 12 field pulses. 6 We conclude that in guinea-pig right atrium auto-inhibitory feed-back plays little role in the modulation of transmitter release at levels of stimulation that cause 50-60% of maximum tissue response. This is because neuronal uptake normally prevents synaptic concentrations of noradrenaline from activating prejunctional c2-adrenoceptors. Stimulation sufficient to induce a nearmaximal response or the presence of neuronal uptake inhibition are necessary to evoke autoinhibitory feed-back. IntroductionThe prejunctional Mc2-adrenoceptor has been considered to be part of an inhibitory feed-back loop whereby transmitter released from sympathetic nerve endings diminishes subsequent transmitter release (Starke, 1977;Rand, McCulloch & Story, 1980;Langer, 1981). Auto-inhibitory feed-back has been thought to modulate transmitter release from pulse to pulse (Rand, Story, Allen, Glover & McCulloch, 1973 Angus & Korner (1980) recently challenged the importance of auto-inhibitory feed-back under moderate conditions of sympathetic stimulation. They found in the guinea-pig isolated right atrium that the tachycardia response was not influenced by pretreatment with phentolamine and yohimbine at sympathetic stimulus strengths that raised the rate up to 50% of the maximum response. This was investigated further by Story et al. (1981) absence of auto-inhibitory feed-back under stimulus conditions similar to those employed by Angus & Korner (1980). But they defined two specific conditions under which sympathetic transmission was altered by auto-inhibitory feed-back: (1) a maximum interval between successive stimuli (4 -8 s) and (2) an adequate length of stimulus train of at least 1.5 s at higher frequencies (2 Hz).Surprisingly with stimulation by 4 pulses Story et al. (1981) observed a U-shaped relationship between the frequency of stimulation and 3H-efflux, which contrasted ...

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Section: Discussionsupporting

confidence: 89%

Section: Specific Activities Of Tissue and Released Noradrenalinesupporting

confidence: 93%

Section: Specific Activities Of Tissue and Released Noradrenalinesupporting

confidence: 87%

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Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Angus¹,

Bobik²,

Jackman³

et al. 1984

British J Pharmacology

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“…This agrees with findings using the same tissue (Henseling et al 1978a(Henseling et al & 1978bSchrold & Nedergaard 1979), rabbit main pulmonary artery (Su & Bevan 1970;Endo er al. 1977;Nedergaard 1980) and dog saphenous vein (BrandHo 1977;Brand50 et al 1980;Verbeuren et al 1978;Muldoon et al 1978;Rorie et al 1980). The contribution of 'H-NA and some of its 'Hmetabolites in the spontaneous outflow from intact aorta was different from that in overflow evoked by electrical-field stimulation (tables 1 and 2).…”

Section: Metabolism Of 'H-na Released Spontaneouslymentioning

confidence: 96%

Effect of Cocaine and Corticosterone on the Metabolism of ³H‐Noradrenaline Released from Rabbit Isolated Aorta and Adventitia

Schrold

Nedergaard

1981

Acta Pharmacologica et Toxicologica

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“…Rorie et al, 1980;Van houtte. 1980], This possibility is ruled out by the fact that cooling reduces the appearance of endogenous transmitter to the same extent as that of 3H-norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

Effect of Moderate Cooling on Adrenergic Neuroeffector Interaction in Canine Cutaneous Veins

Janssens¹,

Verbeuren²,

Vanhoutte³

1981

J Vasc Res

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Experiments were performed to investigate the effect of moderate cooling on adrenergic neuroeffector interaction in canine cutaneous veins. Helical strips of dog’s saphenous vein, untreated or first incubated with ³H-norepinephrine were mounted for superfusion and isometric tension recording; the overflow of endogenous catecholamines or ³H-norepi-nephrine and its metabolites, respectively, were measured in the superfusate. In other experiments the monoamine oxidase activity or the catechol-O-methyltransferase (COMT) activity of the saphenous vein wall was determined. Moderate cooling (from 37 to 24 °C) decreased the evoked release of endogenous norepinephrine during electrical stimulation of the adrenergic nerve endings in the blood vessel wall. Moderate cooling depressed the overflow of ³H-norepinephrine and its metabolites in unstimulated preparations, during electrical stimulation during superfusion with high K⁺ solution and during exposure to tyramine. Moderate cooling reduced the activity of monoamine oxidase significantly more than that of COMT. The relative alterations in overflow of norepinephrine and its metabolites caused by a same degree of cooling in basal conditions and during the different forms of increased overflow of adrenergic transmitter suggest that lowering the temperature inhibits the exocytotic process, but at the same time slows down the diffusion of norepinephrine from the junctional cleft to the extracellular space to the extent that during sympathetic nerve stimulation at 24 °C the effective junctional concentration of the transmitter may be comparable to that obtained at 37 °C. The inhibitory effect of moderate cooling on the extraneuronal metabolism of norepinephrine appears to affect little the effective junctional concentration of the adrenergic transmitter.

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The specific activity of retained and released norepinephrine in dog saphenous vein prelabeled with radiolabeled norepinephrine

Cited by 21 publications

References 19 publications

Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Effect of Cocaine and Corticosterone on the Metabolism of ³H‐Noradrenaline Released from Rabbit Isolated Aorta and Adventitia

Effect of Moderate Cooling on Adrenergic Neuroeffector Interaction in Canine Cutaneous Veins

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The specific activity of retained and released norepinephrine in dog saphenous vein prelabeled with radiolabeled norepinephrine

Cited by 21 publications

References 19 publications

Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in 3H‐efflux and atrial rate in guinea‐pig atrium

Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in 3H‐efflux and atrial rate in guinea‐pig atrium

Effect of Cocaine and Corticosterone on the Metabolism of 3H‐Noradrenaline Released from Rabbit Isolated Aorta and Adventitia

Effect of Moderate Cooling on Adrenergic Neuroeffector Interaction in Canine Cutaneous Veins

Contact Info

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Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Role of auto‐inhibitory feed‐back in cardiac sympathetic transmission assessed by simultaneous measurements of changes in ³H‐efflux and atrial rate in guinea‐pig atrium

Effect of Cocaine and Corticosterone on the Metabolism of ³H‐Noradrenaline Released from Rabbit Isolated Aorta and Adventitia