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However, recent research into the pathophysiology of ascites and HRS has stimulated new enthusiasm in their prevention and treatment. Patients with HRS have hyperdynamic circulatory dysfunction with reduced arterial blood pressure and reduced central blood volume, owing to preferential splanchnic arterial vasodilatation. Activation of potent vasoconstricting systems, including the sympathetic nervous and renin\u2010angiotensin\u2010aldosterone systems, counteracts the arterial vasodilatation and leads to a pronounced renal vasoconstriction with renal hypoperfusion, a reduced glomerular filtration rate, and intense sodium\u2010water retention. Thus prevention of HRS should seek to improve liver function, limit arterial hypotension and central hypovolaemia, and reduce renal vasoconstriction and the renal and interstitial pressures. Portal pressure can be reduced with \u03b2\u2010adrenergic blockers and transjugular intrahepatic portosystemic shunt (TIPS). Precipitating events, like infections, bleeding, and postparacentesis circulatory syndrome, should be treated to avoid further circulatory failure. Improvement in arterial blood pressure and central hypovolaemia can be achieved with vasoconstrictors, such as terlipressin (Glypressin<jats:sup>\u00ae<\/jats:sup>), and plasma expanders such as human albumin. In the future endothelins, adenosine antagonists, long\u2010acting vasoconstrictors, and antileukotriene drugs may play a role in preventing and treating HRS.<\/jats:p>","DOI":"10.1111\/j.1365-2036.2004.02112.x","type":"journal-article","created":{"date-parts":[[2004,8,27]],"date-time":"2004-08-27T17:29:09Z","timestamp":1093627749000},"page":"31-41","source":"Crossref","is-referenced-by-count":37,"title":["Pathogenesis and pathophysiology of hepatorenal syndrome \u2013 is there scope for prevention?"],"prefix":"10.1111","volume":"20","author":[{"given":"S.","family":"M\u00f8ller","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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