Adrenergic receptors classes

Agonists as well as antagonists of (3-adienergic receptors are used for the treatment of a variety of conditions. (3-Adrenergic receptor antagonists belong to the most frequently used classes of dtugs. 

Scheme 6.1 Chemical structures of adrenergic receptor antagonists for generation of antitarget pharmacophores class I (a) and class II (b).

Figure 6.3 Common-feature pharmacophores ofala adrenergic receptor antagonists [16]. Onto each pharmacophore the reference has been mapped, (a) Class I pharmacophore model aligned to prazosin, (b) class II pharmacophore model aligned to compound 10.

Back in 1913, adrenaline was found to cause either constriction or relaxation of blood vessels, depending on the anatomical site. Scientists correctly concluded that there must be two classes of adrenergic receptors. These are termed alpha and beta adrenergic receptors. When adrenaline hits the alpha-type receptor, blood vessel constriction results at the beta-type receptor, blood vessel relaxation results. Thus, adrenaline and noradrenaline are nonspecific agonists (activators) at adrenergic receptors. 

Adrenergic receptor one of several classes of membrane-localized receptors that recognize adrenaline and noradrenaline as agonists. 

The adrenergic receptors (or adrenoceptors) are a class of G-protein coupled receptors, which are the targets of catecholamines. Adrenergic receptors specifically bind their endogenous ligands, the catecholamines, epinephrine, and norepinephrine (also called adrenaline and noradrenaline), and are activated by these. 

Mechanism of action - Disopyramide is a class lA antiarrhythmic agent that decreases the rate of diastolic depolarization (phase 4), decreases the upstroke velocity (phase 0), increases the action potential duration of normal cardiac cells, and prolongs the refractory period (phases 2 and 3). It also decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium and does not affect alpha- or beta-adrenergic receptors. 

The adrenal medulla synthesizes two catecholamine hormones, adrenaline (epinephrine) and noradrenaline (norepinephrine) (Figure 1.8). The ultimate biosynthetic precursor of both is the amino acid tyrosine. Subsequent to their synthesis, these hormones are stored in intracellular vesicles, and are released via exocytosis upon stimulation of the producer cells by neurons of the sympathetic nervous system. The catecholamine hormones induce their characteristic biological effects by binding to one of two classes of receptors, the a- and )S-adrenergic receptors. These receptors respond differently (often oppositely) to the catecholamines. 

There are two classes of a-adrenergic receptors, aj and a2. Agents with the greatest affinity for aj blockade are chlorpromazine, thioridazine, and risperidone. There are no known beneficial effects associated with a -adrenergic receptor antagonism. However, aj-adrenergic receptor blockade can lead to hypotension, dizziness, and reflex tachycardia (Table 26.2). a2 Blockade is modest for most agents except for risperidone and clozapine. As with aj receptors, there are no benefits that have yet to be associated with a2 receptor... 

Although the SSRIs provided a tremendous advantage over the TCAs in terms of tolerability, an effect on norepinephrine also has some theoretical advantages. For example, some authors have suggested that dual reuptake inhibitors may be more likely to lead to remission (Thase et al. 2001). As the name of the class implies, these agents affect the reuptake of both serotonin and norepinephrine, while having very little effect on muscarinic, histaminic or Hj, or aj-adrenergic receptors. Hence these medications share many of the tolerability and safety benefits of the SSRIs. Currently, two serotonin-norepinephrine reuptake inhibitors (SNRIs) are available in the United States venlafaxine and duloxetine. 

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