Acute administration of captopril lowers the natriuretic and diuretic response to a loop diuretic in patients with chronic cardiac failure

Abstract

Angiotensin-converting enzyme inhibitors suppress plasma concentrations of the sodium retaining hormones angiotensin II and aldosterone. This action should potentiate the natriuretic and diuretic effects of loop diuretics. Some studies indicate, however, that the introduction of angiotensin-converting enzyme inhibitors for the treatment of cardiac failure is associated with transient weight gain and the development of oedema. We have compared the natriuretic and diuretic response to intravenous frusemide 40 mg alone with the natriuretic and diuretic response to intravenous frusemide 40 mg following the administration of a single dose of captopril in 12 supine male patients with stable chronic cardiac failure. Captopril lowered the 4 h diuretic response to frusemide from 1160 (60) to 685 (77) ml (P less than 0.05) and the natriuretic response from 120 (9.6) to 68 (11.7) mmol (P less than 0.05). Creatinine clearance fell after captopril from 91 (7.2) to 57 (7.7) ml min-1 (P less than 0.05). Systolic and diastolic blood pressures were lower after the administration of captopril but these changes were not significant. Plasma renin activity rose from 3.8 (1.04) to 12.34 (2.94) ng ml h-1 (P less than 0.05) and plasma angiotensin II was reduced from 24.9 (5.05) to 8.14 (1.8) pg ml-1 (P less than 0.05). Plasma aldosterone concentrations were not significantly lower following captopril. Angiotensin-converting enzyme inhibitors cause an acute fall in creatinine clearance which may reduce the effects of loop diuretics and attention must be paid to diuretic dosage when initiating angiotensin-converting enzyme inhibitors for the treatment of cardiac failure.

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults

“…190,252 Clinical experience in patients who are hemodynamically or clinically unstable suggests that the hypotensive effects of ACE inhibition may attenuate the natriuretic response to diuretics and antagonize the pressor response to intravenous vasoconstrictors. 301,302 As a result, in such patients (particularly those who are responding poorly to diuretic drugs), it may be prudent to interrupt treatment with the ACEI temporarily until the clinical status of the patient stabilizes.…”

Everything we always wanted to know about furosemide but were afraid to ask

“…Conversely, data about the natriuresis in response to furosemide in the absence and presence of inhibitors of the RAS is limited and not consistent. Two studies indicated that the fractional sodium excretion was diminished when the angiotensin-converting enzyme (ACEi) captopril was acutely administered before furosemide in humans with heart failure; however, the captopril dose led to substantial hypotension (48,101). Motwani et al (107) observed that an ultralow dose of captopril (1 mg), which did not decrease MAP in heart failure patients, enhanced the natriuretic actions of furosemide, whereas a higher dose (25 mg) decreased MAP and attenuated the natriuresis.…”

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

“…Clinical experience in patients who are hemodynamically or clinically unstable suggests that the hypotensive effects of ACE inhibition may attenuate the natriuretic response to diuretics and antagonize the pressor response to intravenous vasoconstrictors (200,201). As a result, in such patients (particularly those who are responding poorly to diuretic drugs), it may be prudent to interrupt treatment with the ACEI temporarily until the clinical status of the patient stabilizes.…”