[Respiratory effects of antihypertensive agents acting on alpha adrenergic receptors]

There are several factors involved in the bronchial muscle tone regulation, such as biochemical, nervous and humoral mechanisms. In general, in chronic obstructive bronchopneumopathy there is a reduction in air flow, due to different physiopathologic factors which, alone or combined, produce these disorders. In particular, according to suggestive hypotheses, it seems that asthma is due to a partial or complete block of beta-receptors with a prevalence of alpha-receptors and subsequent bronchial hypertonicity and hyperactivity, while in patients with allergic asthma a deficiency of beta-2-adrenergic system and an hyperresponsiveness of alpha-adrenergic and/or cholinergic system have been suggested. In relation to this part, alpha-1 antagonist drugs demonstrated to have a bronchodilator effect, thanks to their mechanism of action. Examples of this class of drugs are prazosin, indoramin, and an analogous of prazosin, doxazosin, which has a high antagonist and selective action for post-synaptic alpha-1 adrenergic receptors and a longer half-life. Several and recent observations show that these drugs do not interfere with the respiratory function principal parameters, both in healthy and in asthmatic or chronic bronchopathy subjects, but produce an appreciable improvement of these parameters. Presynaptic alpha-2-adrenergic receptors agonist drugs would mainly act by inhibiting the central nervous system, with a subsequent lower stimulation of post-synaptic alpha-1-adrenergic receptors. Examples of this class of drugs are clonidine, rilmenidine and guanabenz (but, in this case, the effects on the respiratory function are more controversial).(ABSTRACT TRUNCATED AT 250 WORDS)