Circulating endogenous vasoactive intestinal polypeptide (VIP) in patients with uraemia and liver cirrhosis

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Abstract
The concentration of vasoactive intestinal polypeptide (VIP) in peripheral venous plasma was median 6·0 pmol l‐1 (range 0–20) in 112 normal subjects. In fifty‐three patients with decreased kidney function plasma VIP was significantly increased (median 15·0 pmol l‐1, range 0·5–70, P < 0·0001) and positively correlated to serum creatinine concentration (r= 0·51, P < 0·001). In 133 patients with liver cirrhosis peripheral venous VIP was slightly elevated (median 7·0 pmol l‐1 range 0–86, P < 0·01). Samples obtained during a central venous catheterization showed significant renal extraction of circulating VIP in control subjects (median extraction fraction 23%, P < 0·05, n= 6) and in patients with cirrhosis (median 60%, P < 0·02, n= 8), but not in uraemic patients (median 0%, NS n= 5). In control subjects and patients with cirrhosis the concentration of VIP in the hepatic vein was significantly below that of systemic plasma (–42%, P < 0·05, n= 6 and –45%, P < 0·01, n= 10, respectively). On the contrary, in uraemic patients hepatic venous VIP was almost similar to systemic VIP (–4%, NS, n= 7). The results indicate that in normal subjects and patients with cirrhosis both the liver and kidneys are involved in the biodegradation of VIP. The elevated level of circulating VIP in uraemic patients may in part be due to decreased renal and hepatic biodegradation but increased neuronal release of VIP, especially in the splanchnic system, may also contribute to the increased plasma VIP in this condition.