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Results for “Neuroeffector Junction”

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At least 505 records · Page 28Linked to original sources
PubMed1979

[Innervation of the small intestinal mucosa of laboratory animals. II. Ultrastructure of neuro-cellular connections].

In addition to our light microscopic contribution (Stach, Hung 1978) giving an insight into the density, architecture, histochemical variety and relations between plexus mucosus and Lieberkühn's glands the herewith presented electron microscopic results reveal mainly neuro-cellular relations from the lamina propria. This means that the plexus mucosus has mainly the function to innervate blood vessels and lymphatics as well as smooth muscle cells and connective tissue cells (mast cells, histiocytes, plasma cells) of the small intestine mucosa.

Animals↗
PubMed1984

Neuroeffector transmission of the hepatic and pancreatico-duodenal isolated arteries of the dog.

Direct evidence has been obtained that the neurogenic responses of the hepatic and pancreatico-duodenal arteries of the dog are mainly due to norepinephrine released from varicosities and that this effect is mediated via alpha 1-adrenoceptors. In addition, there is a prazosin-resistant response to nerve stimulation that is certainly not mediated via alpha 2-adrenoceptors. These vessels are 10-100 times less sensitive to applied norepinephrine than the great majority of peripheral arteries; however, the pA2 value for prazosin (7.5) is the same as in other systems. The varicose terminal plexus is located deep in the media, as shown by electron microscopic study. Findings indicate that these gastrointestinal arteries are mainly controlled by adrenergic innervation, that their density is as high as that of any other vessel, and that these arteries might be much less influenced by the circulating catecholamines than others. The neuroeffector transmission of hepatic and pancreatico-duodenal arteries is subject to presynaptic modulation. Muscarinic (oxotremorine) and P1 (adenosine) receptor agonists are effective inhibitors of transmission, whereas xylazine surprisingly has no effect.

Animals↗
PubMed1984

Limitations of presynaptic theory: no support for feedback control of autonomic effectors.

Only limited evidence, much of it repetitious, has supported the hypothesis that transmitter release is regulated by negative and positive feedback. It is shown here that the theory fails to satisfactorily predict the outcome of experimental tests that examine transmitter efflux critically, over an array of test conditions in several effector organs. Experimentally established inadequacies relate to: the observed effects of agonists and antagonists on stimulation-induced efflux; presynaptic site specificity; per pulse output of transmitter in the absence and presence of drugs; single-pulse stimulation; synaptic dimensions and efflux; lack of coincidence between enhancement of efflux and blockade of amine-induced inhibition and between effector response size and efflux alterations. Theoretical considerations about negative and positive feedback that render their routine operation unlikely are also discussed. It is concluded that, despite repeated observations that norepinephrine and some antagonists exert presynaptic actions to decrease and enhance transmitter output, the unitary hypothesis that assigns these effects to interactions with functional autoinhibitory and excitatory systems mediated by alpha- and beta-adrenergic receptors is probably not correct.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

[Sequelae of a drug block and the potential for pharmacological correction of the neuroeffector effects on the heart in reversible ischemia of varying duration].

The development of local reversible ischemia of the myocardium is characterized by the stereotyped time course of changes in the heat neuromediator content: predominant increase in the noradrenalin content in the hyperkinetic stage of the disease and fall in its content with concurrent increase in the acetylcholine content in the hypokinetic stage. Cardiac function changes accordingly. Partial blockade of M-cholino- and beta-adrenoreceptors leads to impaired balance of the neuroeffector influences on the heart under irreversible ischemia. The impairment is shown by more material changes in cardiac activity as compared to those induced by concurrent switch-off of the receptors. Pharmacological correction of sympathetic neuroeffector influences by means of myoephedrine increases heart resistance to its reversible ischemic alteration.

Animals↗
PubMed1982

Termination of responses to sympathetic nerve stimulation and to noradrenaline in a perfused arterial preparation: the role of neuronal and extraneuronal uptake.

Perfused branch vessels of bovine radial artery in vitro responded to sympathetic nerve stimulation and to noradrenaline added extralumenally and intralumenally with constrictions monitored as flow reductions. Cocaine and 17 beta-estradiol, inhibitors of neuronal and extraneuronal uptake, respectively, enhanced responses to exogenous noradrenaline given by either route. An analysis of response recovery rates, namely termination of action, revealed that the extraneuronal and neuronal uptake process each accounted for between 35 to 50% of the total inactivation capacity of the perfused neuroeffector system for noradrenaline. Responses to periarterial nerve stimulation over a 0.5 to 10 Hz frequency range, involving minimal to moderate flow reductions, were substantially magnified by cocaine and by 17 beta-estradiol. An analysis of response duration and recovery rates showed that extraneuronal processes were more significant than neuronal uptake in terminating noradrenergic transmitter action over the frequency band of 0.5 to 10 Hz.

Animals↗
PubMed1984

Presynaptic alpha-receptor control of adrenergic transmitter release in blood vessels.

The presynaptic alpha-adrenergic receptor control of transmitter release in vascular tissues is discussed. A model of adrenergic innervation of the vascular bed is proposed based on ultrastructural and histochemical evidence. Evidence is presented to support the concept of intermittent or periodic release of norepinephrine (NE) from the varicosity. Intermittency combined with a mechanism such as presynaptic control to ensure spatial distribution of release sites, along with a slow effector response and recovery, results in a smooth, generalized change in tone and an overall economy of transmitter. The effective concentration of NE around the presynaptic membrane is maintained for considerably less than 0.1 s. It is argued that the transient presence of transmitter in the synapse combined with intermittency of release does not favor accumulation of transmitter at the cleft at physiological frequencies or desensitization of presynaptic receptors. In addition, intermittency provides an explanation for why exogenous NE is more effective presynaptically in influencing release than endogenous NE. The importance of cleft width in presynaptic control of transmitter release, the possible complications caused by facilitation, and resolution of some apparent problems with the presynaptic hypothesis are also discussed.

Action Potentials↗