Beta-adrenergic agonists systemic

The methylxanthines consist of aminophylline, dyphyl-line, enprofylline, and pentoxifylline. Aminophylline (theophylline ethylenediamine) is the most widely used of the soluble theophyllines. Its main therapeutic effect is bronchodilation. In addition, it causes central nervous system stimulation, cardiac acceleration, diuresis, and gastric secretion. Aminophylline is available in an oral, rectal (pediatric), or intravenous solution, which is used in the treatment of status asthmaticus. Although aminophylline is a less effective bronchodilator than beta-adrenergic agonists, it is particularly useful in preventing nocturnal asthma. 

In terms of the noradrenergic system, this chapter has described the locus co-eruleus as that part of the brain containing the noradrenergic neurons that mediate some of the symptoms of anxiety through alpha 2 and beta adrenergic receptors. Our discussion has also extended to the role of serotonin in anxiety, which appears to be key, yet quite complex and incompletely understood. One current theory developed in this chapter is the notion that anxiolytic drugs act as partial agonists at serotonin 1A receptors. 

Enantiomer Preparations of Inhaled Drugs. There has been much interest in the differences in effects of enantiomers of many medications, and beta agonist adrenergic bronchodilators have received much attention. Evidence suggests that the (R)-enantiomer of albuterol is mainly responsible for bronchodilation while the (S)-enantiomer may stimulate airway reactivity. Data suggest, however, that after aerosol delivery, the systemic absorption for (R)-albuterol is faster than for (S)-albuterol and that, conversely, the lung retention of (S)-albuterol is longer, which may be detrimental [29]. The extent to which enantiomers will displace racemic preparations is not yet determined. 

I. Pharmacology. Norepinephrine is an endogenous catecholamine that stimulates mainly alpha-adrenergic receptors. It is used primarily as a vasopressor to increase systemic vascular resistance and venous return to the heart. Norepinephrine is also a weak beta-1-adrenergic receptor agonist, and it may increase heart rate and cardiac contractility in patients with shock. Norepinephrine is not effective orally and is erratically absoihed after subcutaneous injection. After intravenous administration, the onset of action is nearly immediate, and the duration of effect is 1-2 minutes after the infusion is discontinued. 

The tricyclics and some related antidepressants block or inhibit the uptake of noradrenaline (norepinephrine) into adrenergic neurones. Thus the most important means by which noradrenaline is removed from the adrenoceptor area is inactivated and the concentration of noradrenaline outside the neurone can rise. If more noradrenaline (or one of the other directly acting alpha or alpha/beta agonists) is then given, the adrenoceptors of the cardiovascular system concerned with raising blood pressure become grossly stimulated by this superabundance of amines, and the normal response becomes exaggerated. 

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