Lowered albumin extravasation rate in heart but not in other organs in beta3-integrin-deficient mice

The vascular protein permeability is dependent on the integrity of the vascular wall. The heart capillaries in male mice lacking beta3 integrins have an immature phenotype. Previously, we have demonstrated a role for alphavbeta3 integrins in control of interstitial fluid pressure (Pif) and thereby in the fluid flux during inflammation. We wanted to explore a possible role for alphavbeta3 integrins in controlling capillary protein permeability during control situation and inflammation.

We performed double-tracer and microdialysis experiments on beta3-integrin-deficient mice and wild type control mice. We also measured blood pressure and heart rate in the two mice strains.

We found reduced albumin extravasation (during 25 min) in the heart capillaries (0.053 +/- 0.003 vs. 0.087 +/- 0.009 mL g(-1) dw, P < 0.05), and an increased cardiac mass/body weight (5.3 x 10(-3) +/- 0.3 x 10(-3) vs. 3.8 x 10(-3) +/- 0.1 x 10(-3), P < 0.01) in the beta3-integrin-deficient mice (n = 6) compared with the controls (n = 6). Heart rate and blood pressure were the same in mice with and without beta3-integrins. No difference in permeability was found in other tissues studied, or under local inflammation.

These results show a function for the alphavbeta3 integrin in the regulation of protein permeability, selective for the heart capillaries.