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General 3-Adrenoceptor stimulant

Cyclic AMP accumulation by catecholamines is generally associated with /3-adrenoceptor stimulation, but there is recent evidence that a adrenoceptor stimulation also can lead to cyclic AMP accumulation. For example, in slices of rat cerebral cortex, the effect of isoprenaline on the cyclic AMP level was inhibited by a /3-adrenoceptor blocking drug and yet inhibition of the effect of noradrenaline required the combination of a P and an a-adrenoceptor blocking drug [65,66]. [Pg.301]

Amino alcohols, such as /S-agonists and /S-blockers, are chiral hy-droxyl-arnine-contairiing compounds. Most of the amino alcohols are marketed as racemic mixtures. In general, for these /S-agonists, only the (R)-enantiomers are potent /3-adrenoceptor stimulants with little or no activity attributed to the (S)-enantiomers (55). [Pg.29]

In general, the responses to administered catecholamines are similar to those seen after sympathetic nerve stimulation and depend on the type of adrenoceptor in the muscle. [Pg.102]

Thus, it seems that the lack of sympathetic nervous system inhibition produced by the vasodilators, which is advantageous in some ways, can also be a disadvantage in that reflex increases in sympathetic nerve activity will lead to hemodynamic changes that reduce the effectiveness of the drugs. Therefore, the vasodilators are generally inadequate as the sole therapy for hypertension. However, many of the factors that limit the usefulness of the vasodilators can be obviated when they are administered in combination with a -adrenoceptor antagonist, such as propranolol, and a diuretic. Propranolol reduces the cardiac stimulation that occurs in response to increases in sympathetic nervous activity, and the... [Pg.227]

The best-characterized action of the adrenoceptor agonists in the airways is relaxation of airway smooth muscle. Although there is no evidence for direct sympathetic innervation of human airway smooth muscle, ample evidence exists for the presence of adrenoceptors on airway smooth muscle. In general, stimulation of 32 receptors relaxes airway smooth muscle, inhibits mediator release, and causes tachycardia and skeletal muscle tremor as adverse effects. [Pg.430]

It has been demonstrated that the / -selectivity is due to the para-substituents of /(-adrenoceptors. In contrast, (-)-erythro-isoetliarine, a bronchodilator. is 80 times more selective for ft -adrenergic receptors than for ft-receptors, lsoetharine contains ancr-alkyl substituent, thus producing four isomeric compounds. The (-)-erythro isomer is 100-1 old more active than the (-)-threo isomer and has more than 500 times the activity of either of the (+)-isomers and in blocking electrically stimulated spasms. In general, introduction of a-alkyl substituents on both /1-blockers and agonists provides diastereomers with increased ft-selectivity, but often with compromised potency. [Pg.1268]

More broadly, timolol therapy should be considered with caution in patients with any significant sign, symptom, or history for which systemic beta-blockade would be medically imwise.This includes disorders of cardiovascular or respiratory origin (e g., asthma, chronic bronchitis, and emphysema) as well as many other conditions. Spirometric evaluation after institution of timolol therapy may help to identify patients in whom bronchospasm develops after commencement of therapy. In general, however, patients with asthma and other obstructive pulmonary diseases should avoid this drug. Sympathetic stimulation may be essential to support the circulation in individuals with diminished myocardial contractility, and its inhibition by P-adrenoceptor antagonists may precipitate more severe cardiac feilure. [Pg.150]

Comprehensive reviews about the chemistry and pharmacology of ephedra and its use in sports and weight loss products have recently been published.The pharmacological effects of maHUANG are generally attributed to ephedrine, which include central nervous system (CNS) stimulation, peripheral vasoconstriction, elevation of blood pressure, bronchodilatation, cardiac stimulation, decrease of intestinal tone and motility, mydriasis, and tachycardia, among others (zhou). The central stimulant action of ephedrine appears to be mediated by /-adrenoceptors and not by dopamine receptors. ... [Pg.266]


See other pages where General 3-Adrenoceptor stimulant is mentioned: [Pg.497]    [Pg.574]    [Pg.24]    [Pg.31]    [Pg.74]    [Pg.470]    [Pg.1]    [Pg.28]    [Pg.36]    [Pg.185]    [Pg.47]    [Pg.274]    [Pg.278]    [Pg.25]    [Pg.37]    [Pg.186]    [Pg.650]    [Pg.1410]    [Pg.37]    [Pg.320]    [Pg.70]    [Pg.32]    [Pg.67]    [Pg.139]    [Pg.335]    [Pg.158]    [Pg.24]    [Pg.30]    [Pg.248]    [Pg.764]    [Pg.2662]    [Pg.393]    [Pg.717]    [Pg.1152]    [Pg.207]    [Pg.252]   
See also in sourсe #XX -- [ Pg.29 ]




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