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2 edition of Some effects of bretylium on adrenergic nerve function in rat heart. 1972. found in the catalog.

Some effects of bretylium on adrenergic nerve function in rat heart. 1972.

Christopher J. Pycock

Some effects of bretylium on adrenergic nerve function in rat heart. 1972.

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Published .
Written in English


Edition Notes

Ph. D. thesis of the Councilfor National Academic Awards.

ID Numbers
Open LibraryOL13660013M

9. Effects of Adrenergic Neurone Blocking Agents on the Responses of Sympathetic Neuroeffectors to Acetylcholine or Nerve Stimulation and on the Release of Noradrenaline.- IV. Morphological and Physiological Evidence for an Interaction between Cholinergic and Adrenergic Nerve Terminals.- V. The Role of Ca2+ for the Noradrenaline-Releasing. α - and β-adrenergic receptor selectivity. Adrenergic agonists have been developed which exhibit binding and activation preference for one or another adrenergic receptor type. Some agents bind preferably to α-receptors while others exhibit selectivity for β-receptors. For the case of agonists, binding is associated with receptor activation; therefore, binding selectivity for agonists. Therefore, these results imply that 18 F-LMI has the potential to be a new class of assay to facilitate research into the understanding of cardiac norepinephrine uptake-2 mechanism in various heart diseases and might be used for monitoring the effects of medication on the norepinephrine uptake in rat models.


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Some effects of bretylium on adrenergic nerve function in rat heart. 1972. by Christopher J. Pycock Download PDF EPUB FB2

Bretylium caused a specific and lasting depression of many excitatory and inhibitory responses evoked by electrical stimulation of the peripheral sympathetic nervous system, probably by impairing conduction of impulses in adrenergic neurones with consequent failure of noradrenaline and adrenaline by:   Results 3 1 Rat mortality While there were no deaths of newborn rats treated with bretylium there was a 60% mortality of adult rats 3 2 Fluorescence htstochemastry Visual observations showed no change in the density or intensity of fluorescence of the adrenergic innervation of the iris, vas deferens and atrium of newborn or adult rats during Cited by: 3.

Some effects of bretylium on adrenergic nerve function in rat heart. Author: Pycock, C. ISNI: Open University Date of Award: Availability of Full Text: Full text unavailable from EThOS.

Restricted access. ofnoradrenaline and on adrenergic nerve function in rat heart E. ABBSAND C. PYCOCK* Department of Pharmacology, School of Pharmacy, Portsmouth Polytechnic, Portsmouth, POI 2DZ, Hants.

Summary 1. The effects of bretylium were investigated on the content and subcellular distribution of noradrenaline in therat heart andonthe response to Cited by: The effects of bretylium on the subcellular distribution of noradrenaline and on adrenergic nerve function in rat heart.

Brit. Pharmacol. 49, 11–22 (). Effects of some adrenergic neuron blockers, related quaternary ammonium compounds and guanidine derivatives on degenerating adrenergic nerves in the conscious rat.

Acta physiol Cited by: Download Citation | Biochemical properties of bretylium | The effect of bretylium (10−3m) on the respiration of brain slices and certain enzyme systems has been investigated.

This concentration. The Effect of Age on Adenosine A 1Receptor Function in the Rat Heart. is related to an action of bretylium on the adrenergic nerve terminal.

effects of muscle, nerve and neuromuscular. Christopher J. Pycock has written: 'Some effects of bretylium on adrenergic nerve function in rat heart. Adrenergic stimulation—by epinephrine in the blood and by norepinephrine released from sympathetic nerve endings—has both excitatory and inhibitory heart, dilatory muscles of the iris, and the smooth muscles of many blood vessels are stimulated to contract.

The smooth muscles of the bronchioles and of some blood vessels, however, are inhibited from contracting; adrenergic. Adrenergic drug 1) inhibits NE nerve function and produces cardiovascular effects similar to reserpine (treat hypertension) 2) However, its action is complex, involving inhibition of excitation-secretion coupling perhaps by preventing normal action potential-induced fusion of.

Bretylium and tetracaine when perfused at increasing concentrations inhibited and finally blocked discharges elicited by acetylcholine and KCl in adrenergic nerve endings of the isolated perfused heart and less regularly in the isolated perfused spleen of the cat. There was a direct correlation between the inhibition of the effects of sympathetic nerve stimulation and the inhibition of KCl.

Psychiatric side effects including confusion, anxiety, psychoses, and emotional lability have been reported rarely. A causal relationship between the side effect and the use of bretylium has not been clearly established. giachetti, r.a. hollenbeck, extra‐vesicular binding of noradrenaline and guanethidine in the adrenergic neurones of the rat heart: a proposed site of action of adrenergic neurone blocking agents, british journal of pharmacology, /jtbx, 58, 4, (), ().

The relation between the adrenergic neurone-blocking and noradrenaline-depleting actions of some guanidine derivatives. Br J Pharmacol. Jun; 51 (2)– [Europe PMC free article] [Google Scholar] Abbs ET, Pycock CJ. The effects of bretylium on the subcellular distribution of noradrenaline and on adrenergic nerve function in rat heart.

Effects of Bretylium, Related Quaternary Ammonium Compounds, and Mitosis Inhibitors on the Degeneration Activity in the Sympathetically Innervated Periorbital Smooth Muscle in the Conscious Rat Noradrenaline Nerve Terminals in the Rat Cerebral Cortex following Lesion of the Dorsal Noradrenaline Pathway: A Study on the Time Course of their.

Sympathetic adrenergic nerves innervate the SA and AV nodes, conduction pathways, and myocytes in the heart. These adrenergic nerves release the neurotransmitter norepinephrine (NE), which binds to specific receptors in the target tissue to produce their physiological responses.

Neurotransmitter binding to receptors activates signal transduction pathways that cause the observed changes in. Nils‐Erik Andé, Matts Henning, Hopé Obianwu, Effect of Epsilon Amino Caproic Acid on Adrenergic Nerve Function and Tissue Monoamine Levels, Acta Pharmacologica et Toxicologica, /jtbx, 26, 2, (), ().

The adrenergic innervation of the pulmonary vasculature of the file snake Acrochordus granulatus was examined by use of glyoxylic acid-induced fluorescence. Perivascular plexuses of blue-green fluorescent nerves are observed around the common pulmonary artery, the anterior and posterior pulmonary arteries, the arterioles leading to the gas exchange capillaries of the lung, the venules draining.

In a later publication Abbs and Pycock () reported similar findings with the rat heart; they observed a correlation in time between the bretylium-induced depletion of noradrenaline from the microsomal fraction and adrenergic neuron blockade. Effects of bretylium bier block and handgrip exercise on mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity bursts.

Values are means ± SE for 8 subjects. bpm, Beats/min. Muscle sympathetic nerve activity was higher post-bretylium; however, MAP and HR were not significantly changed by the intervention.

Comparison of bretylium and guanethidine: tolerance, and effects on adrenergic nerve function and responses to sympathomimetic amines. Br J Pharmacol Chemother. Aug; – [PMC free article] Briant RH, Reid JL. Desmethylimipramine and the hypotensive action of clonidine in the rabbit.

Br J Pharmacol. Nov; 46 (3)P–P. adrenergic nerve ending; NE. Location of Alpha 2 receptors and ligand. heart. Effect of beta 1 activation on heart rate.

increase. Effect of beta 1 on force of contraction (inotropic effect) increase in BP. Increase of renin by beta 1 causes. increases air flow via bronchodilation.

SOME NOVEL EFFECTS OF PROGES-TERONE Pages with reference to book, From 68 To 71 A. Qayum, S.M. Yusuf (Dept. of Paediatric Surgery, National Institute of Chlid Health, Jinnah Postgraduate Medical Center, Karachi.) Besides its usual physiological effects on the endometrium, breast and vagina, it has been found that.

The adrenergic system is one system with lots of receptors that can be stimulated, and many effects that can occur. These nerve cells use epinephrine and norepinephrine as biochemical messengers.

An adrenergic nerve fibre is a neuron for which the neurotransmitter is either adrenaline (epinephrine), noradrenaline or dopamine. These neurotransmitters are released at a location known as the synapse, which is a junction point between the axon of one nerve cell and the dendrite of another.

The neurotransmitters are first released from the axon and then bind to the receptor site on the. The advantage of a local application of bretylium was the avoidance of any systemic drug effects. LDF was monitored from the bretylium-treated and control sites.

The key to this approach is that the presynaptic blockade of norepinephrine release by bretylium blocks the vasoconstrictor system and leaves the active vasodilator system unaltered. Drugs which affect the synthesis or storage of noradrenaline will affect all sympathetic nerves, thereby causing a diverse range of effects.

In addition, because there is an overlap in the mechanisms involved in the synthesis, storage, release and removal of noradrenaline, adrenaline and dopamine, drugs which affect noradrenergic neurotransmission will have similar effects on adrenergic and.

ANS receptors: Adrenergic receptors: In the ANS, adrenergic neurons release NA which binds with adrenergic receptors and propogate the nerve impulses. The two main types of adrenergic receptors are α-receptors & β-receptors.

These receptors further subclassified as α- α1, α2 and β- β1, β2, β3. Interestingly, however, bretylium increased heart rate, resulting in a negative resting adrenergic tonus (–%), and we were unable to demonstrate that catecholamines supported cardiac function at rest or at circulating concentrations approximating those following an exhaustive chase (adrenaline, 21 nmol l–1; noradrenaline, 14 nmol l–1).

Adrenergic nerve fibre, nerve fibre that releases the neurotransmitter norepinephrine (also known as noradrenaline) at the synapse, or junction, between a nerve and its end organ, which may be a muscle, gland, or another rgic nerve fibres make up the sympathetic nervous system, one of two peripheral nervous systems controlling involuntary activities, such as digestion, respiration.

Effect of Beta Receptor Activation on the Heart: Activation of the beta 1 receptor leads to increases in contractile force and heart stimulation by catecholamines can induce significant increases in heart rate and hmias are a major concern with drugs such as E, NE and ISO that can activate the beta 1 receptor.

Effect of Beta Receptor Activation on Smooth Muscle. arrhythmia - abnormal electrical pattern of the heart (abnormal ekg/ abnormal heart rhythm) anti-arrhythmics - medications intended to restore normal electrical heart pattern bretylium, in an.

ADRENERGIC STIMULATION ANATOMY The release of epinephrine in the blood or norepinephrine released from the sympathetic nerve endings constitutes adrenergic stimulation which can have both the effect of enhancement or inhibition on the body.

STIMULATION Stimulation which requires contraction, such as the heart, dilation of the muscles which affect the iris, and smooth muscles which are found. While the role of the adrenergic nervous system in the progression of left ventricular failure has been well established, its contribution to the pathogenesis of pulmonary arterial hypertension (PAH) and the resultant right ventricular failure is far less clear.

The earliest attempts to treat PAH included drugs that were α-adrenergic agonists such as tolazoline [1] and isoproterenol [2. The contro olf heart rat bey the autonomic nervous syste wams investigate d in conscious human subject by observins g the effect os f /3-adrenergic blockade with propranolol o parasympathetif, c blockade an witd ohf atropine com- bined sympatheti ancd parasympathetic blockade The increas.

ien heart rate. Adrenergic signal transduction: This schematic shows the mechanism of adrenergic receptors. Adrenaline and noradrenaline are ligands to α1, α2, or β-adrenergic receptors. α1-receptors couple to Gq, resulting in increased intracellular Ca2+ and causing smooth muscle contraction.

α2 receptors couple to Gi, causing a decrease in cAMP activity. Professor of pharmacology, the United States, published a book of adrenergic neurotransmission in Raymond Ahlquist, in Georgia, but its meaning will be ignored by the time mainly.

However, because he incorporate textbook of pharmacology in medicine, their findings of the drill inadrenaline / also firmly – it was able to establish.

1 Effects of (−)‐, (±)‐, and (+)‐propranolol, atenolol, guanethidine, bretylium and tetracaine were studied on relaxation responses of rabbit ileum and contractile responses of rabbit pulmonary artery and guinea‐pig vas deferens to electrical nerve stimulation (2 to 50 Hz) 2 In the ileum, inhibition by tetracaine × 10−6M occurred at high frequencies of stimulation, while.

This review addresses open questions about the role of β-adrenergic receptors in cardiac function and failure. Cardiomyocytes express all three β-adrenergic receptor subtypes—β 1, β 2, and, at least in some species, β β 1 subtype is the most prominent one and is mainly responsible for positive chronotropic and inotropic effects of catecholamines.

An adrenergic innervation of the teleost heart was long denied and may in fact be absent in some groups (in, e.g., pleuronectids; Santer ; Donald and Campbell ).

However, the Falck-Hillarp technique has been used to demonstrate an adrenergic innervation of the heart of several species. The current treatment of essential hypertension is based on the following concepts: (1) a single cause has not been identified.

Indeed, essential hypertension appears to be a multifactorial disorder. Specific therapy, therefore, is not possible;1 (2) the homeostatic mechanisms that regulate blood pressure are intact in hypertensive subjects and responsive to physiologic and chemical interventions.A negative inotropic effect has also been reported via activation of β 3 ‐ARs.

β 3 ‐AR activation increases the activity of protein kinase G (PKG) via cyclic guanosine monophosphate (cGMP)‐dependent signalling and thereby modulates both vascular and muscular function of the heart IV. Morphological and Physiological Evidence for an Interaction between Cholinergic and Adrenergic Nerve Terminals.- V.

The Role of Ca2+ for the Noradrenaline-Releasing Effect of Acetylcholine on Adrenergic Nerve Terminals.- VI.

Conclusions.- B. Effects of Catecholamines on Cholinergic Nerve Terminals.- I. Effects on Transmission in Autonomic.