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Biomedical subjects

F J Stefano

Publications and source records attributed to F J Stefano.

At least 55 records · Page 3Linked to original sources
PubMed1977

Secretory effects of 6-hydroxydopamine in normal and denervated submaxillary glands of the rat.

Injection of 6-hydroxydopamine (6-OH-DA) elicited a marked and sustained secretory response of control and surgically sympathectomized submaxillary glands of rats. These responses were diminished by previous treatment with reserpine 0.1 mg/kg 48 and 24 h before the experiment and almost abolished by 5 mg/kg reserpine 6 h before the administration of 6-OH-DA. The responses to 6-OH-DA were potentiated in control glands by previous preganglionic denervation of either the parasympathetic or sympathetic nerves of the gland. Development of postjunctional supersensitivity in denervated glands also increased the responses to 6-OH-DA, while atropine had a feeble blocking action. For all these responses, the adrenal catecholamines played no role. After two consecutive doses of 6-OH-DA a third dose of the drug still elicited a secretory response that was 50% of that of the first dose. It is concluded that for the responses to 6-OH-DA the leakage of noradrenaline from the degenerating adrengic nerve endings of the submaxillary gland plays a partial role. Noradrenaline released by the drug from other tissues and reaching the gland via the circulation also contributes to the responses observed. A muscarinic component may also participate in the secretory effects of 6-OH-DA.

Adrenal Medulla↗
PubMed1975

Effects of 6-hydroxydopamine Treatment at birth on the submaxillary gland of the rat.

Six and 18 months after neonatal administration of 6-hydroxy-dopamine or surgical sympathetic denervation the submaxillary gland of the rat showed a marked depletion of noradrenaline stores. Six months afer removal of the superior cervical ganglion the gland's endogenous noradrenaline was lowered to 0.032 +/- 0.004 mug/g while after neonatal 6-hydroxydopamine the values were 0.228 +/- 0.023 mug/g (controls 2.145 +/- 0.382 mug/g). Eighteen months after either type of sympathetic denervation the neurotransmitter was still depleted. In rats treated with 6-hydroxydopamine the sailagogue effect of injected noradrenaline was potentiated 2.7-fold while the potentiation of the effect of noradrenaline was 3.6 times after surgical denervation. The magnitude of the supersensitivity developed to isoprenaline did not differ between both types of denervation. No supersensitivity to the cholinomimetic agent, methacholine, was observed. Cocaine administration or removal of the superior cervical ganglion slightly increased the supersensivity to noradrenaline in rats treated with 6-hydroxydopamine. Eighteen months after surgical or chemical denervation, the activity of choline-acetyl-transferase in the submaxillary gland was increased by about 50%. Of the respiratory enzymes studied, sussinic dehydrogenase, fumarase and cytochrome oxidase, the activity of only the latter was markedly reduced by a chronic sympathetic denervation. From the results obtained it is concluded that neonatal treatment with 6-hydroxy-dopamine causes a permanent and almost complete sympathectomy of the submaxillary gland of the rat.

Aging↗
PubMed1972

Role of the -adrenoceptor in regulating noradrenaline overflow by nerve stimulation.

1. A study of the actions of phenoxybenzamine on transmitter overflow, neuronal and extraneuronal uptake of noradrenaline and in causing alpha-adrenoceptor blockade was carried out using the isolated cat nictitating membrane preparation.2. Phenoxybenzamine increased transmitter overflow elicited by nerve-stimulation at 10 Hz in a concentration dependent manner in the range 10(-8) to 10(-5) g/ml.3. Neuronal uptake of [(3)H]-noradrenaline was not inhibited by concentrations lower than 10(-6) g/ml of phenoxybenzamine. With 10(-7) g/ml of phenoxybenzamine a significant increase in transmitter overflow was obtained, although neuronal uptake of noradrenaline was not affected. Higher concentrations of phenoxybenzamine (10(-6) and 10(-5) g/ml) inhibited the neuronal uptake of noradrenaline and further increased transmitter overflow.4. Extraneuronal uptake of [(3)H]-noradrenaline was inhibited only with the highest concentration of phenoxybenzamine tested (10(-5) g/ml) and therefore appears to be unrelated to the effects on transmitter overflow.5. There was a significant correlation between the degree of alpha-adrenoceptor block produced by phenoxybenzamine and the increase in transmitter overflow obtained by nerve stimulation.6. These results indicate that phenoxybenzamine, in addition to increasing overflow by preventing reuptake of noradrenaline, may increase transmitter release.7. The possibility that phenoxybenzamine acts on alpha-adrenoceptors in the adrenergic nerve terminal is discussed. These receptors would be involved in a negative feedback mechanism regulating transmitter release.

Animals↗
PubMed1969

Tricyclic antidepressants: evidence for an intraneuronal site of action.

Desipramine, a tricyclic antidepressant drug, almost completely prevents the accumulation of tritiated norepinephrine by sympathetic neurons of the rat heart after the injection of a tracer dose of the labeled amine. However, desipramine does not alter the accumulation of norepinephrine after the injection of a large dose of the neurohormone. Despite the failure of desipramine to block the neuronal uptake of norepinephrine, it still prevents exogenous norepinephrine from displacing the endogenous neurohormone (previously labeled with H(3)-norepinephrine) from intraneuronal storage sites.

Animals↗