Acute Effects of Captopril on Systemic and Renal Hemodynamics and on Renal Function in Cirrhotic Patients With Ascites

Pariente, E. A.; Bataille, C; Bercoff, É.; Lebrec, Didier

doi:10.1016/s0016-5085(85)80088-3

Cited by 101 publications

(39 citation statements)

References 17 publications

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“…By activating V1 receptors, it causes splanchnic stimulated to compensate the splanchnic vasodilatationinduced decrease in the effective arterial volume, 27 interfering with RAS could lead to arterial hypotension and renal dysfunction. Consistently, AT-II receptor antagonist salarasin 73 and AT-converting enzyme inhibitor captopril 74 resulted in a marked hypotension in patients with portal hypertension. Treatment for 1 week with 25 mg of losartan, an orally active nonpeptide AT-II antagonist, caused significant decreases in HVPG (approximately 45% reduction of HVPG) in patients with portal hypertension.…”

Section: Current Therapies For Portal Hypertensionmentioning

confidence: 81%

Pathophysiology of Portal Hypertension and Its Clinical Links

Seo¹,

Shah²

2011

Journal of Clinical and Experimental Hepatology

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Section: Current Therapies For Portal Hypertensionmentioning

confidence: 81%

Pathophysiology of Portal Hypertension and Its Clinical Links

Seo¹,

Shah²

2011

Journal of Clinical and Experimental Hepatology

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“…The data also demonstrate that in patients unable to handle their sodiumintake, dopamine level and sodium excretion were increased after chronic captopril administration. Other findings, such as the type of the hormonal profile, interrelation between aldosterone and portal pressure and haemodynamic changes after acute captopril treatment, have previously been described [1,2,7,[11][12][13].…”

Section: Discussionmentioning

confidence: 89%

Portal pressure, renal function and hormonal profile after acute and chronic captopril treatment in cirrhosis

Ibarra

Afione

Garzon

et al. 1992

Eur J Clin Pharmacol

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Summary.The acute effects of captopril in cirrhosis are well known but there are few descriptions of the pattern of response to chronic administration of captopril in this disease. Nine nonuraemic cirrhotic patients with ascites and portal hypertension were studied after 1 week on fixed sodium and water intake (balance diet) and following acute and chronic treatment with captopril (three doses of 25 mg every 30 min and 75 mg. day-~ for three weeks, respectively).Whilst on the balance diet, 7/9 patients were unable to excrete the amount of sodium ingested. After the acute administration of captopril, a significant reduction was seen in arterial blood pressure (86.9 vs 77 mm Hg), with no change in the intra-hepatic pressures (free suprahepatic pressure, FSHP: 15.0 vs 12.1 mmHg and wedged suprahepatic pressure, WSHP: 22.9 vs 20.7 mm Hg).After chronic captopril treatment, a drop was observed in portal pressure (FSHP: 9.4 nunHg and WSHP 18.8 mm Hg, NS) and the arterial pressure returned to its basal level.The plasma aldosterone concentration decreased, whilst noradrenaline and dopamine increased significantly, the latter more than the former, leading to a reduction in the noradrenaline/dopamine ratio (14.5 vs 5.0). Seven out of nine patients showed enhanced natriuresis and the remaining two, who previously had had a positive sodium balance failed to do so. These haemodynamic, hormonal and renal changes were interpreted as evidence of blockade of angiotensin II generation by captopril, and also as a homoeostatic response by the sympathetic nervous system.

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“…Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be avoided in patients with cirrhosis and ascites even in low doses as they can induce arterial hypotension and renal failure [60,61]. If used, blood pressure and renal function must be monitored carefully [7].…”

Section: Drugs To Be Avoided or Used With Cautionmentioning

confidence: 99%

Pharmacological Therapy of Ascites

Ajlan¹,

Al–Hamoudi²,

Elsiesy³

2017

Ascites - Physiopathology, Treatment, Complications and Prognosis

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Ascites refer to accumulation of fluids in the peritoneal cavity. Ascites is caused by multiple causes, among which liver cirrhosis is the commonest. Confirming the etiology is the first and most important step toward proper management. Assuming that ascites is always caused by cirrhosis can lead to unnecessarily sending patients with different etiologies for liver transplantation, particularly patients with non-cirrhotic portal hypertension. Calculating serum albumin ascitic gradient is important in differentiating ascites due to portal hypertension from other etiologies. The first-line therapy for ascites in cirrhosis is low salt diet and diuretics. It is important to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) and nephrotoxic medications in these patients.

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Acute Effects of Captopril on Systemic and Renal Hemodynamics and on Renal Function in Cirrhotic Patients With Ascites

Cited by 101 publications

References 17 publications

Pathophysiology of Portal Hypertension and Its Clinical Links

Pathophysiology of Portal Hypertension and Its Clinical Links

Portal pressure, renal function and hormonal profile after acute and chronic captopril treatment in cirrhosis

Pharmacological Therapy of Ascites

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