ACE inhibitors + Diuretics; Loop, Thiazide and related
The combination of captopril or other ACE inhibitors with loop or thiazide diuretics is normally safe and effective, but ‘first dose hypotension’ (dizziness, lightheadedness, fainting) can occur, particularly if the dose of diuretic is high, and often in association with various predisposing conditions. Renal impairment, and even acute renal failure, have been reported. Diuretic-induced hypokalaemia may still occur when ACE inhibitors are used with these potassium-depleting diuretics.
Clinical evidence
(a) First dose hypotensive reactionThe concurrent use of captopril or other ACE inhibitors and loop or thiazide diuretics is normally safe and effective, but some patients experience ‘first dose hypotension’ (i.e. dizziness, lightheadedness, fainting) after taking the first one or two doses of the ACE inhibitor. This appears to be associated with, and exaggerated by, certain conditions (such as heart failure, renovascular hypertension, haemodialysis, high levels of renin and angiotensin, low-sodium diet, dehydration, diarrhoea or vomiting) and/or hypovolaemia and sodium depletion caused by diuretics, particularly in
high doses. A study describes one woman whose blood pressure of 290/150 mmHg failed to respond to a 10-mg intravenous dose of furosemide.
After 30 minutes she was given captopril 50 mg orally and within 45 minutes her blood pressure fell to 135/60 mmHg, and she required an infusion of saline to maintain her blood pressure.1 In another study, a man developed severe postural hypotension shortly after furosemide was added to captopril treatment.2
Starting with a low dose of the ACE inhibitor reduces the risk of firstdose hypotension. In a study in 8 patients with hypertension, treated with a diuretic (mainly furosemide or hydrochlorothiazide) for at least 4 weeks, captopril was started in small increasing doses from 6.25 mg.
Symptomatic postural hypotension was seen in 2 of the 8 patients, but was only mild and transient.3
Hypotension is more common in patients with heart failure who are receiving large doses of diuretics. In a study in 124 patients with severe heart failure, all receiving furosemide (mean dose 170 mg daily; range 80 to 500 mg daily) and 90 also receiving the potassium-sparing diuretic spironolactone, the addition of captopril caused transient symptomatic hypotension in 44% of subjects. The captopril dose had to be reduced, and in 8 patients it was later discontinued. In addition, four patients developed symptomatic hypotension after 1 to 2 months of treatment, and captopril was also discontinued in these patients.4
There is some evidence that in patients with heart failure the incidence of marked orthostatic hypotension requiring treatment discontinuation in the first 36 hours was lower with perindopril 2 mg once daily than captopril 6.25 mg three times daily (6 of 357 cases versus 16 of 368 cases, respectively).5
high doses. A study describes one woman whose blood pressure of 290/150 mmHg failed to respond to a 10-mg intravenous dose of furosemide.
After 30 minutes she was given captopril 50 mg orally and within 45 minutes her blood pressure fell to 135/60 mmHg, and she required an infusion of saline to maintain her blood pressure.1 In another study, a man developed severe postural hypotension shortly after furosemide was added to captopril treatment.2
Starting with a low dose of the ACE inhibitor reduces the risk of firstdose hypotension. In a study in 8 patients with hypertension, treated with a diuretic (mainly furosemide or hydrochlorothiazide) for at least 4 weeks, captopril was started in small increasing doses from 6.25 mg.
Symptomatic postural hypotension was seen in 2 of the 8 patients, but was only mild and transient.3
Hypotension is more common in patients with heart failure who are receiving large doses of diuretics. In a study in 124 patients with severe heart failure, all receiving furosemide (mean dose 170 mg daily; range 80 to 500 mg daily) and 90 also receiving the potassium-sparing diuretic spironolactone, the addition of captopril caused transient symptomatic hypotension in 44% of subjects. The captopril dose had to be reduced, and in 8 patients it was later discontinued. In addition, four patients developed symptomatic hypotension after 1 to 2 months of treatment, and captopril was also discontinued in these patients.4
There is some evidence that in patients with heart failure the incidence of marked orthostatic hypotension requiring treatment discontinuation in the first 36 hours was lower with perindopril 2 mg once daily than captopril 6.25 mg three times daily (6 of 357 cases versus 16 of 368 cases, respectively).5
(b) HypokalaemiaIn one study, the reduction in plasma potassium was greater with hydrochlorothiazide 25 mg daily than with hydrochlorothiazide combined with cilazapril 2.5 mg daily, showing that cilazapril reduced the potassium-depleting effect of hydrochlorothiazide.6 In one analysis, 7 of 21 patients taking potassium-depleting diuretics given ACE inhibitors for heart failure developed hypokalaemia. This was corrected by potassium supplementation in 2 cases, an increase in the ACE inhibitor dose in 3 cases, and the use of a potassium-sparing diuretic in the remaining 2 cases.7 In another report, a woman taking furosemide 80 to 120 mg daily remained hypokalaemic despite also taking ramipril 10 mg daily and spironolactone 50 to 200 mg daily.8 However, note that the addition of ‘spironolactone’, (p.23) to ACE inhibitors and loop or thiazide diuretics has generally resulted in an increased incidence of hyperkalaemia.
(c) HyponatraemiaAn isolated report describes a patient who developed severe hyponatraemia 3 days after bendroflumethiazide 10 mg daily was added to treatment with enalapril 20 mg daily and atenolol 100 mg daily. However, on 2 other occasions she only developed mild hyponatraemia when given bendroflumethiazide alone.9 An earlier study reported changes in sodium balance due to captopril in all 6 patients with renovascular hypertension and in 11 of 12 patients with essential hypertension; sodium loss occurred in 12 of the 18 patients.1
(d) Impairment of renal functionThe risk of ACE inhibitor-induced renal impairment in patients with or without renovascular disease can be potentiated by diuretics.10-13 In an analysis of 74 patients who had been treated with captopril or lisinopril, reversible acute renal failure was more common in those who were also treated with a diuretic (furosemide and/or hydrochlorothiazide) than those who were not (11 of 33 patients compared with 1 of 41 patients).12
Similarly, in a prescription-event monitoring study, enalapril was associated with raised creatinine or urea in 75 patients and it was thought to have contributed to the deterioration in renal function and subsequent deaths in 10 of these patients. However, 9 of these 10 were also receiving loop or thiazide diuretics, sometimes in high doses.14 Retrospective analysis of a controlled study in patients with hypertensive nephrosclerosis identified 8 of 34 patients who developed reversible renal impairment when treated with enalapril and various other antihypertensives including a diuretic (furosemide or hydrochlorothiazide). In contrast, 23 patients treated with placebo and various other antihypertensives did not develop renal impairment.
Subsequently, enalapril was tolerated by 7 of the 8 patients without deterioration in renal function and 6 of these patients later received diuretics.15 One patient was again treated with enalapril with recurrence of renal impairment, but discontinuation of the diuretics (furosemide, hydrochlorothiazide, and triamterene) led to an improvement in renal function despite the continuation of enalapril.16
Renal impairment in patients taking ACE inhibitors and diuretics has also been described in patients with heart failure. A patient with congestive heart failure and pre-existing moderate renal impairment developed acute non-oliguric renal failure while taking enalapril 20 mg daily and furosemide 60 to 80 mg daily, which resolved when the sodium balance was restored.17 In a study involving 90 patients with severe congestive heart failure who were receiving furosemide and spironolactone, a decline in renal function occurred in 18 patients during the first month after initiation of captopril treatment; mean serum creatinine levels rose from 220 to 300 micromol/L. All the patients were receiving high daily doses of furosemide and all had renal impairment before receiving the first dose of captopril.4
Acute, fatal, renal failure developed in 2 patients with cardiac failure within 4 weeks of being treated with enalapril and furosemide, and in 2 similar patients renal impairment developed over a longer period.18 Reversible renal failure developed in a patient with congestive heart failure when captopril and metolazone were given.19
Similarly, in a prescription-event monitoring study, enalapril was associated with raised creatinine or urea in 75 patients and it was thought to have contributed to the deterioration in renal function and subsequent deaths in 10 of these patients. However, 9 of these 10 were also receiving loop or thiazide diuretics, sometimes in high doses.14 Retrospective analysis of a controlled study in patients with hypertensive nephrosclerosis identified 8 of 34 patients who developed reversible renal impairment when treated with enalapril and various other antihypertensives including a diuretic (furosemide or hydrochlorothiazide). In contrast, 23 patients treated with placebo and various other antihypertensives did not develop renal impairment.
Subsequently, enalapril was tolerated by 7 of the 8 patients without deterioration in renal function and 6 of these patients later received diuretics.15 One patient was again treated with enalapril with recurrence of renal impairment, but discontinuation of the diuretics (furosemide, hydrochlorothiazide, and triamterene) led to an improvement in renal function despite the continuation of enalapril.16
Renal impairment in patients taking ACE inhibitors and diuretics has also been described in patients with heart failure. A patient with congestive heart failure and pre-existing moderate renal impairment developed acute non-oliguric renal failure while taking enalapril 20 mg daily and furosemide 60 to 80 mg daily, which resolved when the sodium balance was restored.17 In a study involving 90 patients with severe congestive heart failure who were receiving furosemide and spironolactone, a decline in renal function occurred in 18 patients during the first month after initiation of captopril treatment; mean serum creatinine levels rose from 220 to 300 micromol/L. All the patients were receiving high daily doses of furosemide and all had renal impairment before receiving the first dose of captopril.4
Acute, fatal, renal failure developed in 2 patients with cardiac failure within 4 weeks of being treated with enalapril and furosemide, and in 2 similar patients renal impairment developed over a longer period.18 Reversible renal failure developed in a patient with congestive heart failure when captopril and metolazone were given.19
(e) Pharmacokinetic and diuresis studies
1. Furosemide. A study in healthy subjects given single doses of enalapril and furosemide found no evidence of any pharmacokinetic interaction between these drugs.20 Another study in hypertensive patients found that captopril did not affect the urinary excretion of furosemide, nor its subsequent diuretic effects.21 However, a further study in healthy subjects showed that, although captopril did not alter urinary excretion of furosemide, it did reduce diuresis.22 Yet another study in healthy subjects found that captopril reduced the urinary excretion of furosemide, and reduced the diuretic response during the first 20 minutes to approximately 50%, and the natriuretic response to almost 30%, whereas enalapril and ramipril did not significantly alter the diuretic effects of furosemide.23 In
one single-dose study in healthy subjects the concurrent use of benazepril and furosemide reduced the urinary excretion of furosemide by 10 to 20%, whereas benazepril pharmacokinetics were unaffected.24 Lisinopril did not alter plasma levels or urinary excretion of furosemide in one study, nor did it alter urinary electrolyte excretion.25 Similarly, furosemide did not affect the pharmacokinetics of lisinopril either in single-dose or multipledose regimens.26
2. Hydrochlorothiazide. In a single-dose, randomised, crossover study in 19 elderly patients the pharmacokinetics of enalapril 10 mg were unaffected by hydrochlorothiazide 25 mg. However, there was a significant reduction in renal clearance and a significant increase in the AUC of its metabolite, enalaprilat, resulting in higher serum levels of the active drug. This acute interaction was not thought to be clinically significant for long-term use.27
No pharmacokinetic interaction occurred between cilazapril and hydrochlorothiazide in healthy subjects or patients with hypertension.6 Similarly, no significant pharmacokinetic interaction occurred between imidapril and hydrochlorothiazide in healthy subjects28 and neither captopril nor ramipril altered the diuresis induced by hydrochlorothiazide.23
The manufacturer of spirapril briefly noted in a review that there was no clinically relevant pharmacokinetic interaction between spirapril and hydrochlorothiazide.
29 Furthermore no pharmacokinetic interaction was found when spirapril and hydrochlorothiazide were given together as a bi-layer tablet.30 There was no clinically important pharmacokinetic interaction when moexipril was given with hydrochlorothiazide in a singledose study in healthy subjects.31
No pharmacokinetic interaction occurred between cilazapril and hydrochlorothiazide in healthy subjects or patients with hypertension.6 Similarly, no significant pharmacokinetic interaction occurred between imidapril and hydrochlorothiazide in healthy subjects28 and neither captopril nor ramipril altered the diuresis induced by hydrochlorothiazide.23
The manufacturer of spirapril briefly noted in a review that there was no clinically relevant pharmacokinetic interaction between spirapril and hydrochlorothiazide.
29 Furthermore no pharmacokinetic interaction was found when spirapril and hydrochlorothiazide were given together as a bi-layer tablet.30 There was no clinically important pharmacokinetic interaction when moexipril was given with hydrochlorothiazide in a singledose study in healthy subjects.31
Mechanism
The first dose hypotension interaction is not fully understood. One suggestion is that if considerable amounts of salt and water have already been lost as a result of using a diuretic, the resultant depletion in the fluid volume (hypovolaemia) transiently exaggerates the hypotensive effects of the ACE inhibitor.
The cases of hypokalaemia are simply a result of the potassium-depleting effects of the diuretics outweighing the potassium-conserving effects of the ACE inhibitor. The converse can also occur.
Thiazides can cause hyponatraemia, but this enhanced effect may have been due to an alteration in renal haemodynamics caused by the ACE inhibitor; sustained angiotensin-converting enzyme blockade can produce natriuresis.1
Marked decreases in blood pressure may affect renal function, and in addition, the renin-angiotensin system plays an important role in the maintenance of the glomerular filtration rate when renal artery pressure is diminished.11 However, diuretic-induced sodium depletion may also be an important factor in the renal impairment sometimes observed with ACE inhibitors.
Importance and management
The ‘first dose hypotension’ interaction between ACE inhibitors and diuretics is well established. The BNF in the UK notes that the risk is higher when the dose of diuretic is greater than furosemide 80 mg daily or equivalent, 32 and suggest that, in patients taking these doses of diuretics, consideration should be given to temporarily stopping the diuretic or reducing its dosage a few days before the ACE inhibitor is added. If this is not considered clinically appropriate, the first dose of the ACE inhibitor should be given under close supervision. In all patients taking diuretics, therapy with ACE inhibitors should be started with a very low dose, even in patients at low risk (e.g. those with uncomplicated essential hypertension on low-dose thiazides). To be on the safe side, all patients should be given a simple warning about what can happen and what to do when they first start concurrent use. The immediate problem (dizziness, lightheadedness, faintness), if it occurs, can usually be solved by the patient lying down. Taking the first dose of the ACE inhibitor just before bedtime is also preferable.
Any marked hypotension is normally transient, but if problems persist it may be necessary temporarily to reduce the diuretic dosage. There is usually no need to avoid the combination just because an initially large hypotensive response has occurred.
A number of products combining an ACE inhibitor with a thiazide diuretic are available for the treatment of hypertension. These products should be used only in those patients who have been stabilised on the individual components in the same proportions.
The use of ACE inhibitors in patients taking potassium-depleting diuretics does not always prevent hypokalaemia developing. Serum potassium should be monitored.
There is only an isolated report of hyponatraemia, but be aware that ACE inhibitors may affect the natriuresis caused by diuretics.
A number of products combining an ACE inhibitor with a thiazide diuretic are available for the treatment of hypertension. These products should be used only in those patients who have been stabilised on the individual components in the same proportions.
The use of ACE inhibitors in patients taking potassium-depleting diuretics does not always prevent hypokalaemia developing. Serum potassium should be monitored.
There is only an isolated report of hyponatraemia, but be aware that ACE inhibitors may affect the natriuresis caused by diuretics.
The cases of renal impairment cited emphasise the need to monitor renal function in patients on ACE inhibitors and diuretics. If increases in blood urea and creatinine occur, a dosage reduction and/or discontinuation of the diuretic and/or ACE inhibitor may be required. In a statement, the American Heart Association comments that acute renal failure complicating ACE inhibitor therapy is almost always reversible and repletion of extracellular fluid volume and discontinuation of diuretic therapy is the most effective approach. In addition, withdrawal of interacting drugs, supportive management of fluid and electrolytes, and temporary dialysis, where indicated, are the mainstays of therapy.13 Combined use of ACE inhibitors, diuretics and NSAIDs may be particularly associated with an increased risk of renal failure, see ‘ACE inhibitors + NSAIDs’, p.28.
The possibility of undiagnosed renal artery stenosis should also be considered.
None of the pharmacokinetic changes observed appear to be clinically significant.
1. Case DB, Atlas SA, Laragh JH, Sealey JE, Sullivan PA, McKinstry DN. Clinical experience with blockade of the renin-angiotensin-aldosterone system by an oral converting-enzyme inhibitor (SQ 14,225, captopril) in hypertensive patients. Prog Cardiovasc Dis (1978) 21, 195–206.
2. Ferguson RK, Vlasses PH, Koplin JR, Shirinian A, Burke JF, Alexander JC. Captopril in severe treatment-resistant hypertension. Am Heart J (1980) 99, 579–85.
3. Koffer H, Vlasses PH, Ferguson RK, Weis M, Adler AG. Captopril in diuretic-treated hypertensive
patients. JAMA (1980) 244, 2532–5.
4. Dahlström U, Karlsson E. Captopril and spironolactone therapy for refractory congestive heart failure. Am J Cardiol (1993) 71, 29A–33A.
5. Haïat R, Piot O, Gallois H, Hanania G. Blood pressure response to the first 36 hours of heart failure therapy with perindopril versus captopril. French General Hospitals National College of Cardiologists. J Cardiovasc Pharmacol (1999) 33, 953–9.
6. Nilsen OG, Sellevold OFM, Romfo OS, Smedsrud A, Grynne B, Williams PEO, Kleinbloesem CH. Pharmacokinetics and effects on renal function following cilazapril and hydrochlorothiazide alone and in combination in healthy subjects and hypertensive patients. Br J Clin Pharmacol (1989) 27 (Suppl 2), 323S–328S.
7. D’Costa DF, Basu SK, Gunasekera NPR. ACE inhibitors and diuretics causing hypokalaemia. Br J Clin Pract (1990) 44, 26–7.
8. Jolobe OM. Severe hyperkalaemia induced by trimethoprim in combination with an angiotensin converting enzyme inhibitor in a patient with transplanted lungs. J Intern Med (1997) 242, 88–9.
9. Collier JG, Webb DJ. Severe thiazide-induced hyponatraemia during treatment with enalapril. Postgrad Med J (1987) 63, 1105–6.
10. Watson ML, Bell GM, Muir AL, Buist TAS, Kellett RJ, Padfield PL. Captopril/diuretic combinations in severe renovascular disease: a cautionary note. Lancet (1983) ii, 404–5.
11. Hoefnagels WHL, Strijk SP, Thien T. Reversible renal failure following treatment with captopril and diuretics in patients with renovascular hypertension. Neth J Med (1984) 27, 269–74.
12. Mandal AK, Markert RJ, Saklayen MG, Mankus RA, Yokokawa K. Diuretics potentiate angiotensin converting enzyme inhibitor-induced acute renal failure. Clin Nephrol (1994) 42, 170–4.
1. Case DB, Atlas SA, Laragh JH, Sealey JE, Sullivan PA, McKinstry DN. Clinical experience with blockade of the renin-angiotensin-aldosterone system by an oral converting-enzyme inhibitor (SQ 14,225, captopril) in hypertensive patients. Prog Cardiovasc Dis (1978) 21, 195–206.
2. Ferguson RK, Vlasses PH, Koplin JR, Shirinian A, Burke JF, Alexander JC. Captopril in severe treatment-resistant hypertension. Am Heart J (1980) 99, 579–85.
3. Koffer H, Vlasses PH, Ferguson RK, Weis M, Adler AG. Captopril in diuretic-treated hypertensive
patients. JAMA (1980) 244, 2532–5.
4. Dahlström U, Karlsson E. Captopril and spironolactone therapy for refractory congestive heart failure. Am J Cardiol (1993) 71, 29A–33A.
5. Haïat R, Piot O, Gallois H, Hanania G. Blood pressure response to the first 36 hours of heart failure therapy with perindopril versus captopril. French General Hospitals National College of Cardiologists. J Cardiovasc Pharmacol (1999) 33, 953–9.
6. Nilsen OG, Sellevold OFM, Romfo OS, Smedsrud A, Grynne B, Williams PEO, Kleinbloesem CH. Pharmacokinetics and effects on renal function following cilazapril and hydrochlorothiazide alone and in combination in healthy subjects and hypertensive patients. Br J Clin Pharmacol (1989) 27 (Suppl 2), 323S–328S.
7. D’Costa DF, Basu SK, Gunasekera NPR. ACE inhibitors and diuretics causing hypokalaemia. Br J Clin Pract (1990) 44, 26–7.
8. Jolobe OM. Severe hyperkalaemia induced by trimethoprim in combination with an angiotensin converting enzyme inhibitor in a patient with transplanted lungs. J Intern Med (1997) 242, 88–9.
9. Collier JG, Webb DJ. Severe thiazide-induced hyponatraemia during treatment with enalapril. Postgrad Med J (1987) 63, 1105–6.
10. Watson ML, Bell GM, Muir AL, Buist TAS, Kellett RJ, Padfield PL. Captopril/diuretic combinations in severe renovascular disease: a cautionary note. Lancet (1983) ii, 404–5.
11. Hoefnagels WHL, Strijk SP, Thien T. Reversible renal failure following treatment with captopril and diuretics in patients with renovascular hypertension. Neth J Med (1984) 27, 269–74.
12. Mandal AK, Markert RJ, Saklayen MG, Mankus RA, Yokokawa K. Diuretics potentiate angiotensin converting enzyme inhibitor-induced acute renal failure. Clin Nephrol (1994) 42, 170–4.
13. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy. A statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation (2001) 104, 1985–91.
14. Speirs CJ, Dollery CT, Inman WHW, Rawson NSB, Wilton LV. Postmarketing surveillance of enalapril. II: Investigation of the potential role of enalapril in deaths with renal failure. BMJ (1988) 297, 830–2.
15. Toto RD, Mitchell HC, Lee H-C, Milam C, Pettinger WA. Reversible renal insufficiency due to angiotensin converting enzyme inhibitors in hypertensive nephrosclerosis. Ann Intern Med (1991) 115, 513–19.
16. Lee H-C, Pettinger WA. Diuretics potentiate the angiotensin converting-enzyme inhibitor associated acute renal dysfunction. Clin Nephrol (1992) 38, 236–7.
17. Funck-Brentano C, Chatellier G, Alexandre J-M. Reversible renal failure after combined treatment with enalapril and frusemide in a patient with congestive heart failure. Br Heart J (1986) 55, 596–8.
18. Stewart JT, Lovett D, Joy M. Reversible renal failure after combined treatment with enalapril and frusemide in a patient with congestive heart failure. Br Heart J (1986) 56, 489–90.
19. Hogg KJ, Hillis WS. Captopril/metolazone induced renal failure. Lancet (1986) 1, 501–2.
20. Van Hecken AM, Verbesselt R, Buntinx A, Cirillo VJ, De Schepper PJ. Absence of a pharmacokinetic interaction between enalapril and frusemide. Br J Clin Pharmacol (1987) 23, 84–7.
21. Fujimura A, Shimokawa Y, Ebihara A. Influence of captopril on urinary excretion of furosemide in hypertensive subjects. J Clin Pharmacol (1990) 30, 538–42.
22. Sommers De K, Meyer EC, Moncrieff J. Acute interaction of furosemide and captopril in healthy salt-replete man. S Afr Tydskr Wet (1991) 87, 375–7.
23. Toussaint C, Masselink A, Gentges A, Wambach G, Bönner G. Interference of different ACE-inhibitors with the diuretic action of furosemide and hydrochlorothiazide. Klin Wochenschr (1989) 67, 1138–46.
24. De Lepeleire I, Van Hecken A, Verbesselt R, Kaiser G, Barner A, Holmes I, De Schepper PJ. Interaction between furosemide and the converting enzyme inhibitor benazepril in healthy volunteers. Eur J Clin Pharmacol (1988) 34, 465–8.
25. Sudoh T, Fujimura A, Shiga T, Tateishi T, Sunaga K, Ohashi K, Ebihara A. Influence of lisinopril
on urinary electrolytes excretion after furosemide in healthy subjects. J Clin Pharmacol (1993) 33, 640–3.
26. Beermann B. Pharmacokinetics of lisinopril. Am J Med (1988) 85 (Suppl 3B) 25–30.
14. Speirs CJ, Dollery CT, Inman WHW, Rawson NSB, Wilton LV. Postmarketing surveillance of enalapril. II: Investigation of the potential role of enalapril in deaths with renal failure. BMJ (1988) 297, 830–2.
15. Toto RD, Mitchell HC, Lee H-C, Milam C, Pettinger WA. Reversible renal insufficiency due to angiotensin converting enzyme inhibitors in hypertensive nephrosclerosis. Ann Intern Med (1991) 115, 513–19.
16. Lee H-C, Pettinger WA. Diuretics potentiate the angiotensin converting-enzyme inhibitor associated acute renal dysfunction. Clin Nephrol (1992) 38, 236–7.
17. Funck-Brentano C, Chatellier G, Alexandre J-M. Reversible renal failure after combined treatment with enalapril and frusemide in a patient with congestive heart failure. Br Heart J (1986) 55, 596–8.
18. Stewart JT, Lovett D, Joy M. Reversible renal failure after combined treatment with enalapril and frusemide in a patient with congestive heart failure. Br Heart J (1986) 56, 489–90.
19. Hogg KJ, Hillis WS. Captopril/metolazone induced renal failure. Lancet (1986) 1, 501–2.
20. Van Hecken AM, Verbesselt R, Buntinx A, Cirillo VJ, De Schepper PJ. Absence of a pharmacokinetic interaction between enalapril and frusemide. Br J Clin Pharmacol (1987) 23, 84–7.
21. Fujimura A, Shimokawa Y, Ebihara A. Influence of captopril on urinary excretion of furosemide in hypertensive subjects. J Clin Pharmacol (1990) 30, 538–42.
22. Sommers De K, Meyer EC, Moncrieff J. Acute interaction of furosemide and captopril in healthy salt-replete man. S Afr Tydskr Wet (1991) 87, 375–7.
23. Toussaint C, Masselink A, Gentges A, Wambach G, Bönner G. Interference of different ACE-inhibitors with the diuretic action of furosemide and hydrochlorothiazide. Klin Wochenschr (1989) 67, 1138–46.
24. De Lepeleire I, Van Hecken A, Verbesselt R, Kaiser G, Barner A, Holmes I, De Schepper PJ. Interaction between furosemide and the converting enzyme inhibitor benazepril in healthy volunteers. Eur J Clin Pharmacol (1988) 34, 465–8.
25. Sudoh T, Fujimura A, Shiga T, Tateishi T, Sunaga K, Ohashi K, Ebihara A. Influence of lisinopril
on urinary electrolytes excretion after furosemide in healthy subjects. J Clin Pharmacol (1993) 33, 640–3.
26. Beermann B. Pharmacokinetics of lisinopril. Am J Med (1988) 85 (Suppl 3B) 25–30.
27. Weisser K, Schloos J, Jakob S, Mühlberg W, Platt D, Mutschler E. The influence of hydrochlorothiazide on the pharmacokinetics of enalapril in elderly patients. Eur J Clin Pharmacol (1992) 43, 173–7.
28. Breithaupt-Grögler K, Ungethüm W, Meurer-Witt B, Belz GG. Pharmacokinetic and dynamic interactions of the angiotensin-converting enzyme inhibitor imidapril with hydrochlorothiazide, bisoprolol and nilvadipine. Eur J Clin Pharmacol (2001) 57, 275–84.
29. Grass P, Gerbeau C, Kutz K. Spirapril: pharmacokinetic properties and drug interactions. Blood Pressure (1994) 3 (Suppl 2), 7–13.
30. Schürer M, Erb K, Junge K, Schäfer HF, Schulz H-U, Amschler S, Krupp S, Hermann R. Drug interaction of spirapril hydrochloride monohydrate and hydrochlorothiazide. Arzneimittelforschung (2003) 53, 414–19.
31. Hutt V, Michaelis K, Verbesselt R, De Schepper PJ, Salomon P, Bonn R, Cawello W, Angehrn JC. Lack of a pharmacokinetic interaction between moexipril and hydrochlorothiazide. Eur J Clin Pharmacol (1996) 51, 339–44.
32. British National Formulary. 53rd ed. London: The British Medical Association and The Pharmaceutical Press; 2007. p. 98–100.
28. Breithaupt-Grögler K, Ungethüm W, Meurer-Witt B, Belz GG. Pharmacokinetic and dynamic interactions of the angiotensin-converting enzyme inhibitor imidapril with hydrochlorothiazide, bisoprolol and nilvadipine. Eur J Clin Pharmacol (2001) 57, 275–84.
29. Grass P, Gerbeau C, Kutz K. Spirapril: pharmacokinetic properties and drug interactions. Blood Pressure (1994) 3 (Suppl 2), 7–13.
30. Schürer M, Erb K, Junge K, Schäfer HF, Schulz H-U, Amschler S, Krupp S, Hermann R. Drug interaction of spirapril hydrochloride monohydrate and hydrochlorothiazide. Arzneimittelforschung (2003) 53, 414–19.
31. Hutt V, Michaelis K, Verbesselt R, De Schepper PJ, Salomon P, Bonn R, Cawello W, Angehrn JC. Lack of a pharmacokinetic interaction between moexipril and hydrochlorothiazide. Eur J Clin Pharmacol (1996) 51, 339–44.
32. British National Formulary. 53rd ed. London: The British Medical Association and The Pharmaceutical Press; 2007. p. 98–100.
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