Vasoactive hormones and autocrine activation of capillary exchange barrier function.

Abstract

Capillary barrier function is subject to changes in Starling forces via hemodynamic status (hydrostatic pressure) or protein milieu of fluids bathing the wall (oncotic pressure). Venular function is sensitive to inflammatory mediators leading to white cell sticking, fluid and formed element extravasation, and flow disruption. Thus, we hypothesized that vasoactive hormones and autocrines alter preferentially the venular-capillary (VC) barrier. Hydraulic conductivity (Lp) of frog mesenteric venular- and true-capillaries (TC) was measured by the modified-Landis technique under control (LpC), then during atrial natriuretic peptide (ANP, 10(-7) to 10(-8) M), bradykinin (BKN, 10(-7) M), acetylcholine (ACh, 10(-6) to 10(-5) M), angiotensin II (AII, 10(-7) M), or norepinephrine (NE, 10(-6) M) perfusion. All agents, except AII or NE, elevated Lp: LpANP/LpC = 2.9 +/- 0.3 (mean +/- SEM; (n = 55), LpBKN/LpC = 3.3 +/- 0.8 (n = 16), LpACh/LpC = 1.6 +/- 0.1 (n = 26), LpAII/LpC = 1.1 +/- 0.2 (n = 8), and LpNE/LpC = 1.1 +/- 0.2 (n = 9). Contrary to our hypothesis, VC and TC responded similarly: 3.0 versus 2.9 for ANP, 3.4 versus 3.2 for BKN, and 1.6 versus 1.6 for ACh, respectively. These data are consistent with putative vasodilators lowering capillary barrier resistance independent from changes in Starling forces.