Background. In addition to its vasoconstricting effects, angiotensin II (Ang II) has also demonstrated the ability to modulate microvessel permeability. We hypothesized that activation of the angiotensin II type 1 receptor (AT1) would increase hydraulic permeability. Methods. Hydraulic permeability (L-p) was measured in rat mesenteric venules using the Landis microocclusion technique. Paired measures of L-p were obtained at baseline and after perfusion with the AT1 agonist, [Sar(1)]-angiotensin II, at 10 mumol/L (n = 6) and 100 mumol/L (n = 6). Activation of the AT1 receptor was also achieved by perfusion with 20 nmol/L Ang II plus the angiotensin II type 2 receptor (AT2) antagonist, PD123319. In these studies, 30 mumol/L (n = 6) and 300 mumol/L (n = 6) of PD123319 were used. Results. [Sar(1)]-angiotensin II increased L-p 2-fold with the 10 mumol/L dose (P = .04) and 4-fold with the 100 mumol/L dose (P < .001). The L-p peak due to [Say(1)]-angiotensin II occurred sooner than the peak observed with Ang II. PD123319 (30 mumol/L) plus 20nmol/L Ang II increased L-p 5-fold (P = .003), while PD123319 (300 mumol/L) plus 20 nmol/L Ang II increased L-p 20-fold (P < .0001). The magnitude of, the effect due to PD123319 (300 mumol/L) plus Ang II (20 nmol/L) was approximately twice the summation of effects due to PD123319 (300 mumol/L) alone and Ang II (20 nmol/L) alone. Conclusions. We conclude that endothelial cell Ang II receptors play an important role in modulating transendothelial fluid flux. Activating the AT1 receptor increases L-p; the AT2 receptor may operate to oppose this action. Pharmacologic manipulation of Ang II receptors may be beneficial during shock states to limit intravascular fluid loss.
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