Norepinephrine pharmacological effects

The L-isomers are the naturally occurring forms of epinephrine and norepinephrine and possess considerably greater pharmacological effects than do the D-isomers. Throughout most of the world, epinephrine and norepinephrine are known as adrenaline and noradrenaline, respectively. 

Amphetamine is an indirectly acting adrenomimetic amine that depends for its action on the release of norepinephrine from noradrenergic nerves. Its pharmacological effects are similar to those of ephedrine however, its CNS stimulant activity is somewhat greater. Both systolic and diastolic blood pressures are increased by oral dosing with amphetamine. The heart rate is frequently slowed reflexively. Cardiac output may remain unchanged in the low- and moderate-dose range. 

The pharmacologic effects of direct agonists depend on the route of administration, their relative affinity for adrenoreceptor subtypes, and the relative expression of these receptor subtypes in target tissues. The pharmacologic effects of indirect sympathomimetics are greater under conditions of increased sympathetic activity and norepinephrine storage and release. 

Phenylephrine is a synthetic sympathomimetic amine structurally similar to epinephrine. It acts primarily on ai receptors and has little or no effect on (3 receptors. A minor part of its pharmacologic effects may be attributed to release of norepinephrine from adrenergic nerve terminals. 

Cocaine exhibits several pharmacologic effects. After local application it acts as an anesthetic by blocking the initiation and conduction of nerve impulses. In addition, it has been shown to block neuronal reuptake of norepinephrine, thus potentiating adrenergic activity. Moderate doses increase heart rate and cause vasoconstriction. The most striking systemic effect of cocaine is central nervous system stimulation. 

The toxicities of the beta blockers are directly related to their pharmacologic effects. These agents block the effects of catecholamines such as epinephrine and norepinephrine on the beta-1 and beta-2 receptors. Beta-1 receptors are located in the heart, kidneys, and eyes. Toxicity is most often due to antagonism of the cardiac beta-1 receptors. 

Regarding the pharmacological effects of theanine, previous reports have indicated a reduction in blood pressure in spontaneously hypertensive rats, a relief from convulsions induced by caffeine, and an influence on the brain levels of norepinephrine, serotonin, 5-hydroxyindoleacetic acid, and dopamine. Moreover, oral intake of theanine results in the generation of a-electric waves in the occipital and parietal regions of the human brain Theanine-induced inhibition of glutamate transporter enhances the activity of an antitumor agent. It increased doxorubicin (DOX)-induced antitumor activity, and confirmed that this action contributed to the increase in the DOX concentration in a tumor with inhibition of the DOX efflux from tumor cells. ... 

Juteau N, Bakri F, Pomies IP, Foulon C, Rigaudy P, Pillion G, Lange G, Genre O, Cron JP. The human saphenous vein in pharmacology effect of a new micronized flavonoidic fraction (Daflon 500 mg) on norepinephrine induced contraction. Int Angiol 1995 14(3 Suppl. 1) 8-13. 

Originally tested in cardiovascular disease, trivastal (x, ET U95) has been proposed as a dopamine receptor stimulant with better oral absorption and longer duration of action than apomorphine. In addition to its direct effect on the receptors the data suggested a weak dopamine and norepinephrine releasing effect. Trivastal blocked caudate EEG spindles as did apomorphine and reduced tremor in monkeys with midbrain lesions . Others have reported its drug dynamics and pharmacological actions . 

Both hormones are pyrocatechol (o-dihydroxybenzene) derivatives, which are easily oxidized. This fact explains the histochemical reaction of the chromaffin tissue. The hormonal content of the adrenal medulla is relatively high (several mg per gm of gland). The two active substances of the adrenal medulla, epinephrine and norepinephrine, are both derivatives of phenyl ethylamine, which possesses strong pharmacologic effects. 

Another theory for the action of stimulant diugs in ADHD involves effects on nonstiiatal monoamine systems. Frontal cortical dopamine, norepinephrine, and serotonin are clearly important in cognitive functioning and impulse control. These neurotransmitters directly modulate reward-related behaviors associated with the striatal dopamine system. Moreover, the amygdala may be pharmacologically influenced leading to enhanced... 

Angiotensin II causes vasoconstriction by direct stimulation of ATj receptors on the vascular smooth muscle. It also enhances release of the neurotransmitter norepinephrine from the sympathetic nerve fibers present in the blood vessels. The vasopressor effects of Ag II may be inhibited pharmacologically in order to decrease TPR and treat hypertension. An important class of orally active drugs is the ACE inhibitors, including captopril and enalopril, which prevent formation of Ag II. More recently, angiotensin receptor antagonists have been developed that act at the vascular smooth muscle. These drugs, which include losartin and valsartan, are also orally active. 

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