Bronchial effects of alpha 2-adrenoceptor agonists and of other antihypertensive agents in asthma

Abstract

The respective prevalence of hypertension and asthma is sufficient for their combined existence to be far from rare. The effects of certain antihypertensive drugs, e.g., alpha 2-adrenoceptor agonists, on the bronchi may be either harmful or beneficial. When inhaled, alpha 2-agonists reduce the immediate bronchial response to allergens, whereas when ingested they aggravate the bronchial response to histamine and all the more so when their effect on the central nervous system is greater. Therefore, there has been much interest in agents such as the new oxazoline derivative, rilmenidine, which has less central effects than clonidine, an imidazoline compound of reference. Calcium antagonists inhibit smooth muscle contraction and release of mast cell inflammatory mediators. In asthmatic subjects, their short-term administration leads to a modest improvement in spontaneous bronchial obstruction, has only a partial protective action against various nonspecific or allergenic stimuli, and slightly reinforces the beneficial effect of beta 2-agonists. Beta-adrenoceptor antagonists aggravate bronchial obstruction and nonspecific bronchial hyperreactivity in asthmatic subjects. These harmful effects are dose-dependent, have even been reported after the administration of eyedrops, and are common to all beta-blockers. Angiotensin-converting enzyme inhibitors increase bronchial hyperreactivity in patients who develop cough during treatment and may, in certain cases, worsen or even induce asthma, probably by opposing inactivation by hydrolysis of tachykinins and of bradykinins.