Adrenoceptor agonists/antagonist

Selective adrenoceptor agonists/antagonists as therapeutic agents... 

Prolonged exposure of -adrenoceptor agonists down-regulates -adrenoceptors, ie, their number decreases and they become less responsive. On the other hand, prolonged exposure to -adrenoceptor antagonists (those without ISA) upregulates -adrenoceptors, ie, their numbers increase and they become more responsive. Therefore, patients on -adrenoceptor blocker therapy should be withdrawn from this medication gradually (40). 

Several clinically used drags, e.g. salbirtamol (a/ -adrenoceptor agonist), propanol (a j3-adrenoceptor antagonist) and the 2-arylpropiotric acids (NSAIDs) are employed in... 

Fig. 12.10 Distributions of three large GPCR-specific ligand groups within the Kohonen map (a) Tachykinin NKl antagonists (1400 compounds), (b) Muscarinic Ml agonists (553 compounds), (c), 63-Adrenoceptor agonists (433 compounds).

Other drugs that are reported to have beneficial effects but which have not undergone such extensive evaluation as the neuroleptics or carbamazepine include the calcium channel antagonists such as verapamil. A small open study has suggested that the alpha2 adrenoceptor agonist clonidine may... 

It is to be expected that a drug with an agonist action at a particular receptor type will interact with antagonists at that receptor. For example, the bron-chodilator action of a selective beta-2-adrenoceptor agonist such as salbutamol will be antagonised by non-selective beta-adrenoceptor antagonsists. 

Handley SL, Mithani S (1984) Effects of alpha-adrenoceptor agonists and antagonists in a maze exploration model for fear-motivated behavior. Naunyn Schmiedebergs Arch Pharmacol 327 1-5... 

Therapeutic advantages resulting from new chemical entities with improved receptor selectivity were mentioned earlier in this chapter and are described in detail in later chapters. Such drugs include a- and B-selective adrenoceptor agonists and antagonists, Hi and H2 antihistamines, nicotinic and muscarinic blocking agents, and receptor-selective steroid hormones. All... 

The release of renin is altered by a wide variety of pharmacologic agents. Renin release is stimulated by vasodilators (hydralazine, minoxidil, nitroprusside), 13-adrenoceptor agonists, cx-adrenoceptor antagonists, phosphodiesterase inhibitors (eg, theophylline, milrinone, rolipram), and most diuretics and anesthetics. This stimulation can be accounted for by the control mechanisms just described. Drugs that inhibit renin release are discussed below. 

Bronchodilation is promoted by cAMP. Intracellular levels of cAMP can be increased by 13-adrenoceptor agonists, which increase the rate of its synthesis by adenylyl cyclase (AC) or by phosphodiesterase (PDE) inhibitors such as theophylline, which slow the rate of its degradation. Bronchoconstriction can be inhibited by muscarinic antagonists and possibly by adenosine antagonists. 

---