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Norepinephrine drugs acting

Some adrenomimetic drugs act both directly and indirectly that is, they release some norepinephrine from storage sites and also directly activate tissue receptors. Such drugs are called mixed-action adrenomimetics. However, most therapeutically important adrenomimetic drugs in humans act either directly or indirectly. [Pg.97]

Because the effector cell receptors (muscarinic, <, and 6) are not blocked, patients receiving ganglion-blocking drugs are fully responsive to autonomic drugs acting on these receptors. In fact, responses may be exaggerated or even reversed (eg, norepinephrine may cause tachycardia rather than bradycardia), because homeostatic reflexes, which normally moderate autonomic responses, are absent. [Pg.166]

By the mid-60s there was a strong consensus that depression, at least in its severe endogenous form, was caused by an abnormal biochemical state consisting of reduced levels of monoamines in the brain. The theory was set out systematically in a well-known paper by Schildkraut (1965), who concentrated on the role of noradrenalin (Schildkraut 1965). Other authors focused on serotonin (Coppen 1967). Schildkraut asserted that some if not all depressions are associated with an absolute or relative deficiency of catecholamines, particularly norepinephrine. .. elation may conversely be associated with an excess of such amines (Schildkraut 1965, p. 509). The primary justification for the theory was the belief that stimulants and antidepressant drugs acted to increase monoamine levels. Schildkraut referred to how the supposed efficacy of imipramine had initially cast doubt on the theory, but the riddle had been solved by Axelrod s research on its ability to block tissue reuptake of noradrenalin. [Pg.132]

Mode of action. Amfetamine acts by releasing noradrenaline (norepinephrine) stored in nerve endings in both the CNS and the periphery. As with all drugs acting on the central nervous system, the psychological effects vary with mood, personality and environment, as well as with dose. [Pg.193]

These drugs act as agonists the regulatory otj-adrenergic receptor, both at the neuronal ending and at the level of the nucleus tractus solitarius (NTS). Thus, release of norepinephrine is decreased. [Pg.123]

In addition to oxytocic activity, these drugs act as partial agonists on alpha-adreneigic receptors, as well as receptors for dopamine and serotonin. They also inhibit norepinephrine reuptake. The degree of each effect varies with the individual drug. [Pg.195]

Dopamine and dobutamine are the positive inotropic agents most often used for the shortterm support of the circulation in advanced heart failure. These drugs act via stimulation of the cardiac myocyte dopamine Dj and adrenergic receptors, leading to stimulation of the G -adenylyl cyclase-cyclic AMP-PKA pathway. Isoproterenol, epinephrine, and norepinephrine, although useful in specific circumstances, have little role in the treatment of heart failure see Chapter 10). [Pg.574]

Maprotiline is chemieally similar to the tricyclic drug desipramine except that it has a tetra-cyelic structure. Maprotiline is almost equivalent to desipramine in terms of its sedative and muscarinic receptor blocking actions but has caused seizures at the top of its recommended dose range. Both drugs act selectively to block the reuptake of norepinephrine. The answer is (D). [Pg.277]

The drug acts as a direct and indirect agonist i.e., it helps in the release of norepinephrine. Besides, it also exerts CNS-stimulatory actions. It has been observed that the ephedrine stereoisomer having essentially the (IR, 2S) absolute configuration exhibits direct activity on the receptors, both a and P, as well as an indirect component. It is worthwhile to state here that the (1S, 2R) entantiomer has primarily an indirect activity. [Pg.384]

The TCAs, such as amitriptyline (Elavil) and dox-epin (Sinequan), inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron. Drug classified as MAOIs inhibit the activity of monoamine oxidase a complex enzyme system that is responsible for breaking down amines. This results in an increase in endogenous epinephrine, norepinephrine and serotonin in the nervous system. An increase in these neurohormones results in stimulation of the CNS. The action of the SSRIs is linked to their inhibition of CNS neuronal uptake of serotonin (a CNS neurotransmitter). The increase in serotonin levels is thought to act as a stimulant to reverse depression. [Pg.282]


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See also in sourсe #XX -- [ Pg.70 , Pg.155 , Pg.173 ]




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Drugs acting

Norepinephrine

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