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Home > Journals > Minerva Medica > Past Issues > Minerva Medica 2005 August;96(4) > Minerva Medica 2005 August;96(4):233-46

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CURRENT ISSUEMINERVA MEDICA

A Journal on Internal Medicine

Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,236

Frequency: Bi-Monthly

ISSN 0026-4806

Online ISSN 1827-1669

 

Minerva Medica 2005 August;96(4):233-46

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Arterial hypertension and chronic liver disease

Henriksen J. H., Møller S.

This review looks at the alterations in the systemic haemodynamics of patients with chronic liver disease (cirrhosis) in relation to essential hypertension and arterial hypertension of renal origin. Characteristic findings in patients with cirrhosis are vasodilatation with low overall systemic vascular resistance, high arterial compliance, increased cardiac output, secondary activation of counterregulatory systems (renin-angiotensin-aldosterone system, sympathetic nervous system, release of vasopressin), and resistance to vasopressors. The vasodilatory state is mediated through adrenomedullin, calcitonin gene-related peptide, nitric oxide, and other vasodilators, and is most pronounced in the splanchnic area. This provides an effective (although relative) counterbalance to raised arterial blood pressure. Subjects with arterial hypertension (essential, secondary) may become normotensive during the development of chronic liver disease, and arterial hypertension is rarely manifested in patients with cirrhosis, even in those with renovascular disease and high circulating renin activity. There is much dispute as to the understanding of homoeostatic regulation in cirrhotic patients with manifest arterial hypertension. This probably includes the combination of vasodilatation and vasoconstriction in parallel.

language: English


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