The relationship between sodium retention, hyperactivity of the neurohumoral vasoactive systems, and ascites formation in cirrhosis is intriguing and still remains a subject of interest and debate. According to the most widely accepted theory, the so-called peripheral arteriolar vasodilatation hypothesis of sodium retention and ascites formation in cirrhosis, the predominant mechanism in the pathogenesis of these abnormalities is the presence of persistent systemic arterial vasodilation leading to arterial hypotension, low peripheral resistance, high cardiac output, and decreased effective arterial blood volume.1 These circulatory abnormalities are detected by arterial and cardiopulmonary baroreceptors which in turn initiate the homeostatic activation of the endogenous neurohumoral systems aimed at maintaining arterial pressure within normal or near normal levels. In the kidneys however homeostatic activation of the vasoactive and sodium retaining systems promotes tubular sodium reabsorption and sodium retention.1 Because the splanchnic vasculature is a major site of arteriolar vasodilatation in cirrhosis, it is not surprising that extravasation of the fluid retained by the kidneys occurs mainly in this compartment, leading to the formation of ascites.

The renin-angiotensin-aldosterone (RAAS) and sympathetic nervous (SNS) systems, together with atrial natriuretic peptide (ANP), …