Commentary
See article on page 847Sodium in preascitic cirrhosis: please pass the salt
| The first 150 words of the full text of this article appear below. |
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
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- Sodium homeostasis with chronic sodium loading in preascitic cirrhosis
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Gut 2001 49: 847-851.[Abstract] [Full Text] [PDF]
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