Background: Angiotensin II (Ang II) is a potent vasoconstrictor that is released during shock and sepsis. It is known to have activity on vascular endothelial cells. We hypothesized that Ang II plays a role in the modulation of fluid flux across the microvascular endothelium.
Materials and methods: Hydraulic permeability (L(p)) is a measure of water flow across the endothelial barrier. L(p) was measured in rat mesenteric venules using the modified Landis micro-occlusion technique. To determine the effect of Ang II in basal states, venules were perfused with control Ringer's and measures of L(p) obtained before and after a subsequent perfusion with 20 ng/ml Ang II (n = 5). In additional studies 10 microM ATP was used to activate the endothelium, thereby increasing the L(p) approximately 3-fold. Measures of L(p) were then obtained before and after a subsequent perfusion with 20 ng/ml Ang II (n = 6).
Results: In the basal state, Ang II significantly increased L(p) from 1.45 +/- 0.29 to 3.45 +/- 0.28 (P = 0.013). Following activation by ATP, Ang II decreased L(p) from 4.51 +/- 0.45 to 3.05 +/- 0.28 (P = 0.02). Units for L(p) are x10(-7) cm s(-1) x cm H(2)O(-1).
Conclusions: Ang II increased microvascular permeability under basal conditions while in the activated state it decreased microvascular permeability. In addition to its vasopressor function this differential action of Ang II in modulating fluid flux across the fsendothelium in basal versus activated states may be of benefit under pathophysiological conditions and may be amenable to pharmacologic manipulation.
(c) 2002 Elsevier Science (USA).