The Renin‐Angiotensin‐Aldosterone System in Cirrhosis

Bernardi, Mauro; Domenicali, Marco

doi:10.1002/9780470987476.ch4

Cited by 19 publications

(23 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Urinary excretion of aldosterone was significantly increased in the nonascitic mice and even more so in the animals with ascites. This is consistent with several studies in patients with early cirrhosis, with normal or moderately elevated circulating renin and aldosterone, [13][14][15] and may actually indicate the presence of effective systemic hypovolemia also in the bile duct-ligated mouse, a mechanism that may work alongside a primary sodium retention in the cortical collecting duct. The present mineralocorticosteroid clamp (adrenalectomy plus steroid infusion) shows very convincingly, in concert with the applied molecular techniques, that sodium retention can take place independently of the presence of aldosterone and without stimulation of the mineralocorticoid receptor.…”

supporting

confidence: 91%

“…Also ignored in the discussion is the substantial evidence supporting effective hypovolemia, and the role of aldosterone in sodium reabsorption in cirrhosis. 13,14 This phenomenon is especially important because the widely recognized clinical effects of spironolactone and amiloride in patients with cirrhosis with sodium retention and ascites 14 cannot be explained by the new mouse model.…”

mentioning

confidence: 99%

See 1 more Smart Citation

A new cholestatic mouse model provides insights into renal reabsorption of sodium

Henriksen

2007

Hepatology

View full text Add to dashboard Cite

supporting

confidence: 91%

mentioning

confidence: 99%

A new cholestatic mouse model provides insights into renal reabsorption of sodium

Henriksen

2007

Hepatology

View full text Add to dashboard Cite

“…As in the current investigation, patients evaluated by Garcìa-Pagàn et al 7 had normal levels of PRA and PAC, a common finding in preascitic cirrhosis. 23 The main finding in the current investigation is that canrenone, in association with 40-and 150-mmol/d-sodium diets, normalizes the cardiac dysfunction of cirrhosis; patients receiving canrenone did not show any reduction in LVEF and CI when subjected to the postural challenge. The mechanisms responsible for the cardiovascular effects of canrenone are uncertain.…”

Section: Discussionmentioning

confidence: 70%

Cardiovascular effects of canrenone in patients with preascitic cirrhosis

et al. 2002

View full text Add to dashboard Cite

In patients with cirrhosis and portal hypertension, standing induces a reduction in cardiac index (CI) and an increase in systemic vascular resistance index. Our previous studies indicate that this abnormal hemodynamic response to standing is due to an altered myocardial function, because cirrhotic patients are unable to compensate for the reduced preload with an increase in left ventricular (LV) ejection fraction (EF) and stroke volume. To evaluate whether the cardiac dysfunction in cirrhosis is influenced by canrenone, an aldosterone antagonist, 8 patients with preascitic, nonalcoholic cirrhosis, and portal hypertension underwent echocardiographic assessment of LV function and systemic hemodynamics and determinations of plasma volume, urinary sodium excretion, and plasma renin activity T he hemodynamic pattern of cirrhosis with portal hypertension, with high blood volume and cardiac output and low systemic vascular resistance (SVR), is thought to play a major role in the development of sodium retention and ascites. 1 Bernardi et al. [2][3][4] showed that this hemodynamic pattern occurs only in the supine position; standing is associated with a reduction in cardiac output and an increase in SVR, that is, a "normalization" of systemic hemodynamics. This response to standing is quite different from that of healthy subjects, who do not show any appreciable changes in either cardiac output or SVR. 2-4 However, "normalization" of systemic hemodynamics during standing is associated with activation of vasoconstricting and sodium retaining systems. 3,4 In patients with preascitic cirrhosis, sodium retention occurs only during standing, 3 whereas, in those with ascites, it occurs in either position but worsens during standing. 4 We recently evaluated cardiovascular function in healthy subjects and cirrhotic patients with ascites and hyperdynamic circulation. 5 When supine, patients had increased left ventricular ejection fraction (LVEF) and cardiac index (CI) and reduced LV end-systolic volume index (LVESVI) and SVR. On standing, LV end-diastolic volume index (LVEDVI) decreased in all subjects. Healthy subjects maintained CI and stroke volume index (SVI) by decreasing LVESVI. In contrast, cirrhotic patients experienced a fall in SVI and CI and a disproportionate increase in arterial elastance (Ea), despite marked

show abstract

“…In patients with advanced cirrhosis and ascites, it is widely accepted that arterial underfilling secondary to vasodilation [3] is the main afferent mechanism leading to the activation of sodium retaining systems [4]. It has been clearly demonstrated that renal sodium retention precedes ascites formation [5][6][7][8][9], but we are still looking for the definition of the afferent signal(s) promoting this abnormality.…”

mentioning

confidence: 99%