The role of central blood volume in the development of sodium retention in portal hypertensive rats

Background & Aims: In portal hypertension, peripheral vasodilatation (PVD) causes Na+ retention as a result of vascular underfilling. The central blood volume is responsible for the vascular filling signals to baroreceptors and volume receptors. The aim of this study was to determine the role of central blood volume in Na+ retention in portal hypertensive rats. Methods: Mean arterial pressure, portal pressure, cardiac output, total peripheral resistance, central blood volume, and extracellular Na+ space were assessed daily in rats after portal vein ligation or sham operation until a hyperdynamic circulatory state developed. Results: On day 1, portal vein-ligated rats had PVD and a diminished central blood volume (1.26 +/- 0.04 vs. 1.47 +/- 0.09 mL/ 100 g body wt; P < 0.05), On day 2, Na+ space increased in portal vein-ligated rats (38.1 +/- 0.5 vs. 33.1 +/- 0.5 mL/100 g body wt; P < 0.01). From day 2 on, normalization of central blood volume and cessation of Na+ retention were observed despite persistent PVD. On day 4, portal vein-ligated rats developed a hyperdynamic circulatory state with a normal central blood volume and persistent PVD. Conclusions: Although total peripheral resistance remains decreased, Na+ retention ceases after central blood volume is normalized. Central blood volume therefore appears to be the signal for Na+ retention. Although PVD persists after Na+ retention ceases, it may contribute to Na+ retention by decreasing central blood volume.