Why does lisinopril make you cough
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Understanding Why Lisinopril Causes Cough
Introduction to Lisinopril-Induced Cough
Lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is widely used to treat hypertension and heart failure. However, a common side effect associated with its use is a persistent dry cough. This article explores the mechanisms behind lisinopril-induced cough and the factors influencing its occurrence.
Mechanism of Lisinopril-Induced Cough
Role of Bradykinin and Substance P
The primary mechanism behind lisinopril-induced cough involves the accumulation of bradykinin and substance P. Lisinopril inhibits ACE, which is responsible for the breakdown of bradykinin, a peptide that can induce cough by stimulating sensory nerve endings in the respiratory tract. The accumulation of bradykinin and substance P in the respiratory tract leads to increased cough reflex sensitivity.
Central Nervous System Involvement
Research indicates that lisinopril can cross the blood-brain barrier and act centrally to potentiate the cough reflex. Microinjections of lisinopril into the caudal nucleus tractus solitarii, a brain region involved in cough reflex modulation, significantly increased cough responses in animal studies. This effect was mediated by the accumulation of bradykinin and substance P, further supporting the central role of these peptides in lisinopril-induced cough.
Incidence and Demographic Factors
Higher Incidence in Women and Non-Smokers
Studies have shown that the incidence of cough is higher in patients treated with lisinopril compared to other antihypertensive agents. For instance, a study reported that 8.5% of patients on lisinopril experienced cough, compared to only 3.1% on nifedipine. Interestingly, women reported cough three times more often than men (12.6% vs. 4.4%), and non-smokers were more likely to report cough than smokers.
Comparison with Other Antihypertensive Agents
Several studies have compared the incidence of cough between lisinopril and other antihypertensive agents. For example, the incidence of cough was significantly higher with lisinopril (60%) compared to telmisartan (15.6%) and placebo (9.7%). Similarly, losartan, another angiotensin II receptor antagonist, was associated with a much lower incidence of cough (29%) compared to lisinopril (72%) .
Conclusion
Lisinopril-induced cough is primarily due to the accumulation of bradykinin and substance P, which sensitize the cough reflex both peripherally and centrally. The incidence of this side effect is notably higher in women and non-smokers. Comparisons with other antihypertensive agents like telmisartan and losartan reveal that these alternatives are associated with a significantly lower incidence of cough, making them suitable options for patients who experience this troublesome side effect with lisinopril. Understanding these mechanisms and demographic factors can help in better managing and potentially mitigating this common adverse effect.
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