SummaryThe role of age, gender, smoking habits and concomitant drug treatment, and type and dose of angiotensin converting enzyme (ACE) inhibitor as prognostic factors for the development of cough during ACE inhibition was investigated in a group of 1591 patients. In 117 of these patients cough was identified as drug related. Logistic regression confirmed that females, nonsmokers and patients treated with enalapril are at greater risk of developing cough. On the other hand, our data provided no evidence for a prognostic role of higher doses of the ACE inhibitor or of concomitant drug treatment; in particular, the use of tJ-adrenoceptor antagonists was not associated with a higher incidence of cough.A subset of patients treated with angiotensin converting enzyme (ACE) inhibitors develop a persistent cough, through a mechanism that is incompletely understood (Berkin 1989;Morice et al. 1989). The reported incidence of this adverse effect ranges from 0.2% (Chalmers et al. 1987;Edwards et al. 1987) to over 30% (Town et al. 1987). The true incidence of ACE inhibitor-related cough probably lies between these extremes and can be identified only by applying an appropriate methodology to collect patients' complaints and to verifY their relationship with drug treatment (Strocchi et al. 1989;Yeo & Ramsay 1990).Some evidence suggests that the occurrence of cough during treatment with ACE inhibitors is related to gender, type of inhibitor and smoking habits (Gibson 1989;Strocchi et al. 1989). The aim of this study was to investigate the incidence of cough and the prognostic value of these factors in a large population of unselected hypertensive patients treated with ACE inhibitors. Patients and MethodsA questionnaire on the use of antihypertensive drugs and the potential for subsequent development of adverse effects was sent to 2197 patients treated with ACE inhibitors during the preceding 5 years. 1591 patients (72.4%) correctly completed the questionnaire and were enrolled in this prospective nonconcurrent study (Lilienfeld 1976). Of the 214 cases of cough reported, 117 were judged to be drug related on the basis of direct patient interviews and the use of the operational identification algorithm proposed by Naranjo et al. (1981): 9 men and 37 women treated with captopril, 27 men and 32 women treated with enalapril, and 2 men and 10 women treated with both ACE inhibitors on separate occasions were identified. Further

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The pressor response to norepinephrine (NE) was assessed in normal renin essential hypertensive patients before and after they were randomly assigned to receive in parallel groups of treatment a single dose of an angiotensin converting enzyme (ACE) inhibitor (captopril or lisinopril) or a prolonged therapy with lisinopril (30-45 days) or with hydrochlorothiazide (9 days). Blood pressure was significantly reduced by all treatments. The pressor response to NE was unchanged after the single administration of the ACE inhibitors, while it was blunted after chronic administration of lisinopril and after the diuretic. On the basis of these results, it is suggested that the attenuation of the sympathetically mediated vasoconstriction may represent an additional mechanism contributing to the antihypertensive effect of ACE inhibitors administered chronically.

The potential interaction between fenoldopam, a DA1 selective agonist, and digoxin has been studied in 10 patients with heart failure (NYHA Class II or III) on chronic digoxin treatment. Plasma levels and urinary recovery of the glycoside were monitored for 24 h before and after 9 days of treatment with fenoldopam 100 mg tid. Fenoldopam caused a small, non-significant decrease in the mean steady state plasma concentration and area under the plasma concentration curve of digoxin. As the clearance of digoxin was unchanged there does not appear to be an interaction between fenoldopam and digoxin at the level of the renal tubule.