Antihypertensive drugs and airway function, with special reference to calcium channel blockade.

The treatment of hypertension in patients with airway dysfunction is a delicate problem. This article focuses on the airway effects of some antihypertensive drugs. Early on, the beta-adrenoceptor antagonists were shown to be hazardous in patients with asthma. Nonselective beta-blockers could induce severe asthma attacks and the bronchodilating effect of beta-agonists was totally blocked. Also, the beta-blockers with partial agonist activity totally blocked the effect of bronchodilating beta-agonists. The selective beta 1-adrenoceptor antagonists were shown to have less pronounced effects on the airways, and it was possible to overcome the beta-blockade in the airways with high doses of beta-agonists. beta-Blockers are contraindicated in asthma patients, even if it is possible to give selective beta 1-adrenoceptor antagonists in some patients together with high doses of beta 2-agonists. Angiotensin converting enzyme (ACE)-inhibitors were recently shown to induce cough and bronchial hyperresponsiveness in some patients. This is probably due to an increased inflammation in the bronchial mucosa as substances (e.g., bradykinin) are not metabolized. Therefore, ACE inhibitors could be hazardous in asthmatic patients, as they can increase the underlying bronchial hyperresponsiveness. Calcium channel blockers were earlier considered to be beneficial in asthma, as it was shown that they had a small relaxant effect on bronchial tone, and could amplify the effect of bronchodilators. In studies of provoked bronchoconstriction, calcium channel blockers were shown to have some protective effect against allergens, histamine, methacholine, or exercise-induced bronchoconstriction. Calcium channel blockers do not have a major place in asthma treatment, but as they have no severe side effects on the airways, they could preferably be given to hypertensive patients with airways disease instead of other antihypertensive agents.