Norepinephrine mimics

Adrenergic dru mimic the activity of the sympathetic nervous system. These dragp also are called sympathomimetic druc s. Epinephrine and norepinephrine are neurohormones produced naturally by the body. Synthetic preparations of these two neurohormones,... 

Traditionally, most affective disorders have been treated with compounds that resemble the neurotransmitters that are deficient or in excess in specific brain regions. The aberrant levels of neurotransmitters (or their receptors), such as norepinephrine, dopamine, acetylcholine, and serotonin, have correlated with behavioral symptoms of schizophrenia, depression, anxiety, sleep disorders, motor dysfunctions, attention difficulties, and cognitive disorders. Most drugs discovered for these disorders resulted from screening compounds directly in rodent behavioral models that mimic the behavior of the disease. In these cases, the molecular target" or mechanism of action was assumed to be the deficiency or excess of a neurotransmitter. 

As previously mentioned, many of the effects of nicotine in the brain are likely to be mediated through neuromodulation, in which nicotine potentiates the release of dopamine, norepinephrine, and serotonin (Picciotto 1998). By selectively activating these neurotransmitters, one might be able to mimic some of the reinforcing effects of nicotine. 

Adrenergic drugs are natural or synthetic compounds that either partially or completely replicate the effects of norepinephrine (noradrenaline), epinephrine (adrenaline), and dopamine, and which cause a biological response similar to the activation of the sympathetic nervous system. They are also referred to as sympathomimeties beeause they mimic the stimulation of the sympathetic nervous system. 

Drugs that mimic the actions of acetylcholine are termed cholinomimetic, and those that mimic epinephrine and/or norepinephrine are adrenomimetic. The cholinomimetic drugs are also called parasympathomimetic drugs. The adrenomimetic drugs are often called sympathomimetic. 

The effects of nicotine on the cardiovascular system mimic those seen after activation of the sympathoadrenal system, and they are principally the result of a release of epinephrine and norepinephrine from the adrenal medulla and adrenergic nerve terminals. These effects include a positive inotropic and chronotropic effect on the myocardium as well as an increase in cardiac output. In addition, both systohc and diastolic blood pressures are increased secondary to stimulation of the sympathoadrenal system. These effects are the end result of a summation of adrenergic and chohnergic stimulation. 

In the heart, the effects on the parasympathetic limb predominate. Thus, cholinesterase inhibitors such as edrophonium, physostigmine, or neostigmine mimic the effects of vagal nerve activation on the heart. Negative chronotropic, dromotropic, and inotropic effects are produced, and cardiac output falls. The fall in cardiac output is attributable to bradycardia, decreased atrial contractility, and some reduction in ventricular contractility. The latter effect occurs as a result of prejunctional inhibition of norepinephrine release as well as inhibition of postjunctional cellular sympathetic effects. 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

Amphetamines not only mimic the action of norepinephrine and dopamine they also boost the levels of these neurotransmitters in a synaptic cleft by blocking their removal. Normally, neurotransmitters are reabsorbed by presynaptic neurons after they have exerted their effect on postsynaptic receptor sites. This process, commonly called neurotransmitter reuptake and illustrated in Figure 14.24, is the body s way of recycling neurotransmitters, molecules that are difficult to synthesize. Special membrane-embedded proteins are required to pull once-used neurotransmitter molecules back into a presynaptic neuron. Amphetamines inactivate norepinephrine and dopamine reuptake proteins by binding to them. As a consequence, the concentration of these stimulating neurotransmitters in the synaptic cleft is maintained at a higher-than-normal level. 

Norephedrine and ephedrine mimic and stimulate the release of the adrenal hormones norepinephrine and epinephrine. Norephinephrine raises heart rate and epinephrine stimulates carbohydrate metabolism resulting in an increased metabolic rate, fatty acids release from lipocytes (fat cells), and a protein sparing effect. Caffeine simply prolongs the effect. 

Morphine, the major active principle of powdered opium, is responsible for the action of opium, although other alkaloids contribute to it. Morphine s toxicity is a result of its extensive effect on the central nervous system (CNS), mainly that of a descending depression. Opiates interact with stereospecific and saturable binding sites primarily located in the CNS. Interaction with these receptors mimics the actions of endogenous enkephalins and endorphins. Their action also appears to involve an alteration in the release of neurotransmitters, such as the inhibition of acetylcholine, norepinephrine, and dopamine. 

The sympathetic branch of the autonomic nervous system (see 15.1 The Nervous System) stimulates cells using the neurotransmitter norepinephrine. Adrenergics (sympathomimetics) mimic actions (Table 15.1) of the sympathetic nervous system. These are referred to as adrenergic agonists because it starts a response at the adrenergic receptor sites. 

Substantial efforts have been devoted to the development of molecular sensors for dopamine. Raymo et al.70 reported a two-step procedure to coat silica particles with fluorescent 2,7-diazapyrenium dications sensing toward dopamine. The analysis of the fluorescence decay with multiple-equilibria binding model revealed that the electron deficient dications and the electron-rich analytes form 1 1 and 1 2 complexes at the particle/water interface. The interfacial dissociation constants of the 1 1 complexes were 5.6mM and 3.6mM for dopamine and catechol, respectively. Dopamine was dominated by the interaction of its electron-rich dioxyarene fragment with the electron-deficient fluorophore in neutral aqueous environments. Ahn et al.71 reported tripodal oxazoline-based artificial receptors, capable of providing a preorganized hydrophobic environment by rational design, which mimics a hydrophobic pocket predicted for a human D2 receptor. A moderate binding affinity, a dissociation constant of 8.2 mM was obtained by NMR titrations of tripodal oxazoline-based artificial receptor with dopamine in a phosphate buffer solution (pH 7.0). Structurally related ammonium ions, norepinephrine, 2-phenylethylamine,... 

Sympathomimetics mimic the action of noradrenaline (norepinephrine), the principal neurotransmitter between the nerve endings of the sympathetic nervous system and the adrenergic receptors of the innervated tissues. They stimulate both alpha-adrenoceptors, causing constriction of smooth muscle and blood vessels, and beta-adrenoceptors, producing bronchodilatation. They are therefore useful in coughs where the tissues of the upper respiratory tract are congested, as they shrink swollen mucosa and open up the airways. 

The naturally occurring catecholamines dopamine (1), norepinephrine (2), and epinephrine(3) (Figure 1) play key roles in neurotransmission, metabolism, and in the control of various physiological processes. For example, norepinephrine is the primary neurotransmitter in the sympathetic nervous system and also functions as a neurotransmitter in the central nervous system. Epinephrine, elaborated by the adrenal gland, has potent effects on the heart, vascular and other smooth muscles. Dopamine is an important neurotransmitter in the central nervous system, and has important peripheral effects in such organs as the kidney and heart. The importance of these effects has made the search for drugs that can mimic, inhibit, or otherwise modulate the effects of these catecholamines an important area of medicinal chemistry. 

The family of receptors that responds to norepinephrine and related compounds are called adrenergic receptors. Adrenergic receptors in the peripheral nervous system are important in the activity of smooth muscle and cardiac muscle and in metabolism. The effect on most smooth muscle is relaxation, whereas the effect on cardiac muscle is to increase the force and rate of contraction. Drugs that mimic the action of norepinephrine are... 

Opiates snch as morphine and codeine are thonght to enhance the release by nenrons of the nenrotransmitter dopamine the release of dopamine leads to a sense of enphoria. These drugs are addictive and are often abused. In general, all antipsychotic medications work by blocking dopamine receptors in the forebrain. Nicotine mimics the action of the nenrotransmitter acetylcholine at receptors having to do with the transmission of signals between antonomic nerve cells and skeletal muscle, see also Caffeine Epinephrine Methylphenidate Neurochemistry Neurotransmitters Norepinephrine. 

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