Influence of MAO-inhibitors on deamination of 3H-norepinephrine in the dog's saphenous vein

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Role of neuronal uptake in the disposition of released [3H]-noradrenaline in the dog's saphenous vein

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Inhibition of norepinephrine release in vascular smooth muscle by acetylcholine. Due to hyperpolarization of adrenergic nerve endings

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Depression by local cooling of 3H norepinephrine release evoked by nerve stimulation in cutaneous veins

Experiments were performed to investigate whether local cooling facilitates adrenergic neurotransmission in the cutaneous vein of the dog. Helical strips of saphenous veins were incubated with 3H norepinephrine and mounted for isometric tension recording and superfusion. The superfusate was collected for measurement of total radioactivity or for chromatographic analysis. Electrical stimulation (2Hz) caused contraction and augmented the efflux of 3H norepinephrine and metabolites. Cooling (from 37 to 28°C) imposed during electrical stimulation caused a further increase in tension, but decreased the amount of 3H norepinephrine and metabolites overflowing into the superfusate. These experiments demonstrate that the potentiating effect of cooling on the response of cutaneous veins to sympathetic nerve stimulation is not associated with facilitation of adrenergic neurotransmission. It probably is due to an altered sensitivity of the vascular smooth muscle to the transmitter.link_to_subscribed_fulltex

Inhibition by acetylcholine of the norepinephrine release evoked by potassium in canine saphenous veins

In the dog's saphenous vein acetylcholine inhibits the norepinephrine release caused by nerve stimulation, but not that caused by tyramine. Experiments were performed to determine whether acetylcholine affects the release of norepinephrine evoked by high K+ concentrations. The authors recorded changes in isometric tension of dog saphenous vein strips. Acetylcholine (5 x 10-9 to 10-6 g/ml) caused dose dependent relaxations during contractions caused by K+ 40 mEq/liter. These relaxations were not depressed by tetrodotoxin (10-7 g/ml), which abolished the response to nerve stimulation, but were inhibited by atropine (10-7 g/ml). Strips of saphenous veins were incubated with [3H]norepinephrine and mounted for superfusion (3 ml/min) and isometric tension recording; the total radioactivity and the amount of intact [3H]norepinephrine present in the superfusate were determined. K+ at 50 mEq/liter increased tension, total radioactivity of the superfusate, and the [3H]norepinephrine efflux; acetylcholine (10-7 g/ml) depressed the contraction and diminished the efflux of [3H]norepinephrine. Increasing the K+ concentration from 50 to 70 mEq/liter augmented both tension and the evoked release of [3H]norepinephrine. Acetylcholine did not significantly alter the release of [3H]norepinephrine evoked by K+ 120 mEq/liter. These experiments show that acetylcholine inhibits the norepinephrine release evoked by potassium ions, as it does during nerve stimulation. The inhibition of adrenergic neurotransmission is not due to interference with action potential electrogenesis, but probably is caused by hyperpolarization of the adrenergic nerve endings.link_to_subscribed_fulltex

Effect of blockade of neuronal uptake on the evoked release of 3H-norepinephrine in the saphenous vein of the dog

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Effects of local cooling on adrenergic neurotransmission in the dog's cutaneous vein

Experiments were performed to investigate whether local cooling facilitates adrenergic neurotransmission in the dog's cutaneous vein. Helical strips of saphenous veins were incubated with 3H norepinephrine, and mounted for isometric tension recording and superfusion. The superfusate was collected for measurement of total radioactivity, or for chromatographic analysis. Electric stimulation (2 Hz) caused contraction and augmented the efflux of 3H norepinephrine and metabolites. Cooling (from 37 to 28° C) imposed during electric stimulation caused a further increase in tension, but decreased the amount of 3H norepinephrine and metabolites overflowing into the superfusate. These experiments demonstrate that the potentiating effect of cooling on the response of cutaneous veins to sympathetic nerve stimulation is not due in part to facilitation of adrenergic neurotransmission, but only reflects the greater affinity of the smooth muscle cells for the liberated transmitter.link_to_subscribed_fulltex

Deamination of released 3H-noradrenaline in the canine saphenous vein

Experiments were designed to determine the effect of monoamine oxidase (MAO) inhibitors on the release and the metabolism of noradrenaline in the canine saphenous vein. Helical strips were incubated with 3H-noradrenaline and mounted for superfusion and measurement of the efflux of labelled transmitter and its metabolites; in certain experiments the tissue content of 3H-noradrenaline and its metabolites was also determined. The MAO-A inhibitor clorgyline, and the non-specific inhibitor pargyline, but not the MAO-B inhibitor deprenyl decreased the appearance of deaminated and O-methylated deaminated metabolites under basal conditions and during electrical stimulation. The MAO-A and the non-specific MAO inhibitor did not decrease the efflux of VMA to the same extent as that of the other deaminated metabolites. During superfusion with etidocaine, an agent causing increased leakage of stored transmitter, clorgyline abolished the appearance of DOPEG. Addition of semicarbazide in preparations treated with pargyline did not affect the efflux of deaminated and O-methylated deaminated metabolites. From the measurement of tissue VMA, it appeared that the efflux of VMA poorly reflects quick changes in the rate of its formation but that formation is abolished by pretreatment with pargyline. These experiments indicate that in the canine saphenous vein: (1) DOPEG is formed mainly in intraneuronal sites, while DOMA, MOPEG and VMA are formed extraneuronally; (2) VMA is retained in the tissue after its formation; and (3) the only subtype of MAO involved in the metabolism of 3H-noradrenaline released from adrenergic nerve endings can be classified as MAO-A.link_to_subscribed_fulltex