Increased arterial compliance in cirrhosis is related to decreased arterial C-type natriuretic peptide, but not to atrial natriuretic peptide.
BACKGROUND
Increased arterial compliance (COMPart) has recently been described in patients with cirrhosis, particularly in advanced disease. The aim of the present study was to relate COMPart with arterial levels of the circulating natriuretic peptides: atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), both of which are vasodilators.


METHODS
Thirty-one patients with cirrhosis, 14 non-cirrhotic patients with circulatory disturbances of the ischaemic and hypertensive type, and 10 healthy controls were investigated during a haemodynamic examination.


RESULTS
The patients with cirrhosis showed the well-known hyperdynamic circulation with elevated cardiac output, low arterial blood pressure, and reduced systemic vascular resistance. COMPart in the patients with cirrhosis (1.30 mL/mmHg) was significantly (P < 0.01) increased compared to that of non-cirrhotic patients (0.99 mL/mmHg) and controls (1.01 mL/mmHg). In the patients with cirrhosis, a significant inverse correlation was found between CNP and COMPart (r = -0.42, P < 0.01), but not between CNP and systemic vascular resistance (r = 0.31, P = 0.08). In the non-cirrhotic patients, CNP had a significant inverse correlation to COMPart (r = -0.68, P < 0.01) and a direct correlation to systemic vascular resistance (r = 0.62, P < 0.02). ANP was not significantly related to COMPart nor to systemic vascular resistance in any of the groups.


CONCLUSIONS
The finding of an inverse relation between CNP and COMPart may suggest that a compensatory down-regulation of CNP occurs in patients with cirrhosis and other types of circulatory disorders when vasodilation persists. Regulation of large and small arteries by CNP may be different in cirrhosis. Arterial ANP is not related to properties of the large or small arteries.
Henriksen
J H
JH
Dept. of Clinical Physiology, Hvidovre Hospital, University of Copenhagen, Denmark. jens.h.henriksen@hh.hosp.dk
Gülberg
V
V
Gerbes
A L
AL
Bendtsen
F
F
Møller
S
S
D000328:Adult; D000368:Aged; D001158:Arteries / Q000503:physiopathology*; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000502:physiology*; D004108:Dilatation, Pathologic / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D020098:Natriuretic Peptide, C-Type / Q000097:blood / Q000502:physiology*; D014652:Vascular Diseases / Q000209:etiology / Q000503:physiopathology*
D020098:Natriuretic Peptide, C-Type; D009320:Atrial Natriuretic Factor