Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

MacDonald, TM; Craig, Kate; Watson, Michael

doi:10.1111/j.1365-2125.1989.tb03561.x

Cited by 20 publications

(5 citation statements)

References 34 publications

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“…The subjects were apparently not in sodium equilibrium since prior to furosemide administration sodium excretion was approximately 0.15 mmol/min, corresponding to approximately 200 mmol/day on daily salt intake below 60 mmol/day. Our observations are in agreement with those of MacDonald et al [7] who observed increased natriuresis after furosemide in subjects treated with ramipril.…”

Section: Discussionsupporting

confidence: 83%

Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection

et al. 1993

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The goal of this study was to quantitate the effect of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection. The study was carried out on low and normal salt intake to assess potential interaction with salt balance. Eighteen healthy normotensive volunteers were examined in a double placebo-controlled parallel group design. Subjects were randomly put on either low-salt (20 mmol/day) or normal-salt (110 mmol/day) diet. In either arm of the diet volunteers were first treated orally with placebo for 1 week and subsequently with 2.5 mg/day of the angiotensin-converting enzyme inhibitor cilazapril for another 1 week. Cumulative 24-h urinary sodium excretion was measured on the 6th day of the respective week after sham injection and on the 7th day after injection of 40 mg furosemide. Compared to pretreatment with placebo, pretreatment with cilazapril resulted in a higher cumulative sodium excretion after furosemide injection (day 7) than after the sham injection (day 6) on both salt intakes. The difference in natriuresis (cilazapril versus placebo) was evident 2 and 3 h after injection of furosemide. Neither the time of onset nor the magnitude of antinatriuresis were affected by cilazapril. Following furosemide angiotensin II increased significantly even after cilazapril pretreatment. Cilazapril tended to reduce urinary furosemide excretion. At any given urinary furosemide concentration, the increment in urinary sodium excretion was significantly greater with cilazapril irrespective of salt intake. The study shows that (a) cilazapril increases furosemide-induced natriuresis irrespective of salt intake, (b) antinatriuresis is not affected by cilazapril, and (c) angiotensin II levels rise after furosemide on cilazapril in therapeutic doses.

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Section: Discussionsupporting

confidence: 83%

Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection

et al. 1993

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“…Because the renal tubules are the main source of renal dopamine, renal parenchymal diseases, namely chronic renal failure, are associated with decreased urinary excretion of dopamine [24][25][26]. On the other hand, some medications, namely angiotensin-converting enzyme inhibitors and frusemide, are also known to influence renal dopamine production [27,28]. There is also some evidence that age correlates negatively with plasma levels of L-DOPA and urinary dopamine [29,30].…”

Section: Discussionmentioning

confidence: 99%

Renal synthesis of dopamine in asymptomatic post-infarction left ventricular systolic dysfunction

et al. 2000

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Left ventricular systolic dysfunction (LVSD) following acute myocardial infarction (AMI), by decreasing renal blood flow, may interfere with renal L-DOPA availability and, consequently, dopamine synthesis. Dopamine of renal origin exerts local natriuretic effects. We studied 17 post-AMI patients with asymptomatic LVSD (ejection fraction < 40%) and 14 without (ejection fraction > or = 40%), measuring 24-h urinary excretions of L-DOPA, dopamine and its metabolites, and plasma levels of the amines, amine derivatives and type-B natriuretic peptide (BNP). Baseline characteristics were well balanced between the two groups. No differences were observed in urinary volume and sodium and creatinine excretions. The group with asymptomatic LVSD presented lower urinary excretion of L-DOPA (66.8 +/- 10.1 versus 115.3 +/- 21.9 nmol x day(-1), P = 0.04), whereas plasma levels of L-DOPA were identical in both groups. Urinary dopamine was similar in the two groups (1124.2 +/- 172.4 versus 1049.0 +/- 146.4 nmol x day(-1), P = 0.86), resulting in higher urinary dopamine/L-DOPA ratios in patients with asymptomatic LVSD (20.4 +/- 3.0 versus 9.9 +/- 0.8, P < 0.001). Plasma levels of BNP were higher in the asymptomatic LVSD group (348.5 +/- 47.3 versus 146.8 +/- 21.9 microg x ml(-1), P = 0.003). Ejection fraction was negatively correlated with both plasma levels of BNP and urinary dopamine/L-DOPA ratios. Renal dopamine production is well preserved in patients with asymptomatic LVSD and increased neurohumoral activation, despite reduced urinary excretion of its precursor. This suggests that renal uptake and/or decarboxylation of L-DOPA is enhanced in this condition, as a compensatory mechanism, contributing to preservation of urinary sodium excretion.

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“…Our experiments provide new information that furosemide modulates RBF in an age‐dependent manner. Renal blood flow is enhanced by furosemide in adult animals and humans; 20,21 this forms the basis of its use in the management of acute tubular necrosis and other diseases of renal origin. Previous experiments in adult animals and humans have provided evidence that this renal haemodynamic response to furosemide results from an increase in prostaglandins of the E series 22 .…”

Section: Discussionmentioning

confidence: 99%

Age-dependent cardiovascular, renal and endocrine responses to furosemide in conscious lambs

Thomson

Smith

2004

Clin Exp Pharmacol Physiol

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1. The present study was performed to investigate some of the physiological responses to furosemide during postnatal maturation. 2. In 1- (n = 8) and 6-week old (n = 10) conscious, chronically instrumented lambs at least 3 days after surgery, three experiments were performed at intervals of 24-48 h and in random order. Various parameters of cardiovascular and endocrine function, as well as cumulative urinary flow rates, were measured before and after intravenous injection of 0 mg/kg (experiment one), 0.25 mg/kg (experiment two; low dose) and 5 mg/kg (experiment three; high dose) furosemide. 3. After high-dose furosemide, mean venous pressure decreased and there was a transient increase in mean arterial pressure in lambs aged 6 weeks. At 1 week of age, heart rate increased after high-dose furosemide and renal blood flow decreased. After high-dose furosemide, plasma renin activity increased in both groups of lambs, although the effects were greater in 1-week-old lambs. Plasma levels of arginine vasopressin increased after high-dose furosemide in lambs aged 1 but not 6 weeks. Cumulative urinary flow rate responses to furosemide were similar in 1- and 6-week-old lambs. 4. These data provide new information that cardiovascular and endocrine responses to furosemide are developmentally regulated.

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Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

Cited by 20 publications

References 34 publications

Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection

Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection

Renal synthesis of dopamine in asymptomatic post-infarction left ventricular systolic dysfunction

Age-dependent cardiovascular, renal and endocrine responses to furosemide in conscious lambs

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