Nerves adrenergic

In a monograph on ephedrine Gaddum has reviewed the differences in the action of adrenaline and ephedrine and has suggested that the latter has the same relation to adrenaline as physostigmine has to acetylcholine, that is, ephedrine inhibits the action of an enzyme system, which normally destroys adrenaline, or the substance closely resembling it, produced by adrenergic nerves. 

Noradrenaline transporters (NAT) are localized in the presynaptic plasma membrane of adrenergic nerve terminals. They belong to a family of proteins with 12 putative transmembrane proteins which are responsible for recycling of released neurotransmitters (noradrena-line/adrenaline, dopamine, serotonin, amino acid transmitters) back into the presynaptic nerve ending. Noradrenaline transporters can be blocked by a number of different antidepressant drags, including tricyclic antidepressants (e.g. desipramine) and selective noradrenaline reuptake inhibitors (e.g. reboxetine). 

The adrenergic dragp produce pharmacologic effects similar to the effects that occur in die body when die adrenergic nerves and the medulla are stimulated. The primary effects of these drugp occur on the heart, the blood vessels, and die smooth muscles, such as die bronchi. A basic knowledge of the nervous system is necessary to understand tiiese drugp and how they work in the body. 

N euro transmitters are chemical substances called neurohormones. These are released at Hie nerve ending that facilitate the transmission of nerve impulses. The two neurohormones (neurotransmitters) of the sympathetic nervous system are epinephrine and norepinephrine Epinephrine is secreted by the adrenal medulla Norepinephrine is secreted mainly at nerve ending of sympathetic (also called adrenergic) nerve fibers (Pig. 22-2). 

Antiadrenergic drugs—drug that block adrenergic nerve fibers. These dm i block the adrenergic nerve fibers within the central nervous system (CNS) or within the peripheral nervous system. 

Studies have now started to clarify the role of histamine Hi and H2 receptors in the cardiovascular manifestations of anaphylaxis. However, histamine can activate H3 and H4 receptors [56, 57]. Levi and coworkers [58-60] identified H3 receptors as inhibitory heteroreceptors in cardiac adrenergic nerve endings. This suggests a mechanism by which endogenous histamine can activate norepinephrine release in normal and ischemic conditions [61,62]. The functional identification ofH3 receptors in the human heart [59] means that these receptors might be directly and/or indirectly involved in the cardiovascular manifestations of anaphylactic reactions. 

Neurotoxin that produces a massive release of transmitters from cholinergic and adrenergic nerve endings resulting in continuous stimulation of muscles. It also induces formation of an ion channel allowing the inward flow of calcium ions into the nerve cell. It is a white powder obtained from the venom of the black widow spider. 

Mercuric chloride may induce catecholamine release from adrenals. The initial phase may be due to amine displacement by the mercury ion but the secondary phase probably involves alteration of membrane structures [95]. Mercury compounds have also been shown to increase the efflux of monoamines from mouse striated slices [96] and from adrenergic nerve fibre terminals [97], the effect being attributed to inhibition of Na /K+-ATPase activity and(or) disruption of intracellular Ca2+ regulatory mechanisms [96]. 

Since the discovery that norepinephrine release at the adrenergic nerve terminal is the mechanism whereby the human body maintains sympathetic tone, medicinal scientists have searched for agents which reduce sympathetic tone through interference with norepinephrine peripherally. Reduction of the effect of norepinephrine should lead to a lowering of blood pressure which might be achieved in the following ways ... 

Although this drug is categorized as a local anesthetic, I have chosen to put it in with the hallucinogens because of the psychotomimetic effects that it produces. Cocaine is not a phenylethyl-amine, but it produces central nervous system arousal or stimulant effects which closely resemble those of the amphetamines, the methylenedioxyamphetamines in particular. This is due to the inhibition by cocaine of re-uptake of the norepinephrine released by the adrenergic nerve terminals, leading to an enhanced adrenergic stimulation of norepinephrine receptors. The increased... 

Following the discovery that xylocholine blocked transmission at sympathetic nerve terminals, intensive chemical and biological investigations of related compounds revealed that various benzyl quaternary ammonium salts were potent and selective inhibitors of adrenergic nerve function. A review of compounds of this type has been published by Copp [239]. A -2-Bromobenzyl-A(-ethyl-A. A-dimethylammonium tosylate (LIII) (bretylium) has been studied extensively [237, 258], and suppression of adrenergic nerve function has been demonstrated in numerous test situations in various animal species. 

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