Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Treatment of hypertension in asthma and COPD

Steven E Weinberger, MD
Norman M Kaplan, MD
Section Editors
George L Bakris, MD
James K Stoller, MD, MS
Peter J Barnes, DM, DSc, FRCP, FRS
Deputy Editors
Daniel J Sullivan, MD, MPH
John P Forman, MD, MSc


The management of hypertension in a patient with asthma or chronic obstructive pulmonary disease (COPD) is a common problem owing to the high prevalence of each condition in the adult population. It may be made difficult by the asthma-exacerbating effect of some antihypertensives. As an example, beta blockers should be used with great caution or not at all in patients with chronic asthma (but not chronic obstructive pulmonary disease) or acute allergic or exercise-induced bronchospasm. The angiotensin-converting enzyme (ACE) inhibitors, among the most widely used antihypertensive drugs, can induce a bothersome cough that, although not damaging to the lungs, often can be confused with cough due to such underlying pulmonary diseases such as asthma and COPD.


In patients with asthma, beta blockers can cause increased bronchial obstruction and airway reactivity, and resistance to the effects of inhaled or oral beta receptor agonists (such as albuterol or terbutaline) [1,2]. Even topical ophthalmic administration of nonselective beta blockers for the treatment of glaucoma has led to asthmatic exacerbations [3]. However, beta blockers appear to be safe in patients with COPD and indeed may reduce mortality and exacerbations [4].

The acute clinical effects of beta-1-selective beta blockers and nonselective beta blockers on pulmonary function in patients with asthma were examined in a systematic review and meta-analysis of 32 randomized trials including 1367 patients [1]. The following findings were noted:

Beta-1-selective beta blockers significantly reduced FEV1 by 7 percent and attenuated the bronchodilator response to inhaled beta-2-selective agonists by 10 percent. In addition, one in eight patients had a 20 percent or greater decrease in FEV1.

Nonselective beta blockers had more profound effects on pulmonary function: FEV1 was significantly reduced by 10 percent, and the bronchodilator response to inhaled beta-2-selective was reduced by 20 percent.

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Feb 01, 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Morales DR, Jackson C, Lipworth BJ, et al. Adverse respiratory effect of acute β-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials. Chest 2014; 145:779.
  2. Benson MK, Berrill WT, Cruickshank JM, Sterling GS. A comparison of four beta-adrenoceptor antagonists in patients with asthma. Br J Clin Pharmacol 1978; 5:415.
  3. Fraunfelder FT, Barker AF. Respiratory effects of timolol. N Engl J Med 1984; 311:1441.
  4. Rutten FH, Zuithoff NP, Hak E, et al. Beta-blockers may reduce mortality and risk of exacerbations in patients with chronic obstructive pulmonary disease. Arch Intern Med 2010; 170:880.
  5. Ind PW, Dixon CM, Fuller RW, Barnes PJ. Anticholinergic blockade of beta-blocker-induced bronchoconstriction. Am Rev Respir Dis 1989; 139:1390.
  6. Israili ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology. Ann Intern Med 1992; 117:234.
  7. Bucknall CE, Neilly JB, Carter R, et al. Bronchial hyperreactivity in patients who cough after receiving angiotensin converting enzyme inhibitors. Br Med J (Clin Res Ed) 1988; 296:86.
  8. Boulet LP, Milot J, Lampron N, Lacourcière Y. Pulmonary function and airway responsiveness during long-term therapy with captopril. JAMA 1989; 261:413.
  9. Kaufman J, Casanova JE, Riendl P, Schlueter DP. Bronchial hyperreactivity and cough due to angiotensin-converting enzyme inhibitors. Chest 1989; 95:544.
  10. Lunde H, Hedner T, Samuelsson O, et al. Dyspnoea, asthma, and bronchospasm in relation to treatment with angiotensin converting enzyme inhibitors. BMJ 1994; 308:18.
  11. Tanaka H, Teramoto S, Oashi K, et al. Effects of candesartan on cough and bronchial hyperresponsiveness in mildly to moderately hypertensive patients with symptomatic asthma. Circulation 2001; 104:281.
  12. Lipworth BJ, McDevitt DG, Struthers AD. Prior treatment with diuretic augments the hypokalemic and electrocardiographic effects of inhaled albuterol. Am J Med 1989; 86:653.
  13. Wong CS, Pavord ID, Williams J, et al. Bronchodilator, cardiovascular, and hypokalaemic effects of fenoterol, salbutamol, and terbutaline in asthma. Lancet 1990; 336:1396.
  14. Bear R, Goldstein M, Phillipson E, et al. Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease. Can Med Assoc J 1977; 117:900.
  15. Barnes PJ. Clinical studies with calcium antagonists in asthma. Br J Clin Pharmacol 1985; 20 Suppl 2:289S.
  16. Schwartzstein RS, Fanta CH. Orally administered nifedipine in chronic stable asthma. Comparison with an orally administered sympathomimetic. Am Rev Respir Dis 1986; 134:262.
  17. Ann Twiss M, Harman E, Chesrown S, Hendeles L. Efficacy of calcium channel blockers as maintenance therapy for asthma. Br J Clin Pharmacol 2002; 53:243.
  18. Patakas D, Maniki E, Tsara V, Dascalopoulou E. Nifedipine treatment of patients with bronchial asthma. J Allergy Clin Immunol 1987; 79:959.
  19. Dinh Xuan AT, Matran R, Regnard J, et al. Comparative effects of rilmenidine and clonidine on bronchial responses to histamine in asthmatic subjects. Br J Clin Pharmacol 1988; 26:703.