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There are basically two types of branching patterns in the terminal part of the arteriolar tree. On the one hand, in a number of tissues, including the developing chick embryo chorioallantoic membrane (CAM), the pattern is dichotomous, whereas in other tissues many arteriolar-arteriolar connections, arcades, are found. The structure of the branching pattern depends on the local physical and chemical environment. The goal of this study was to investigate whether substances with an effect on vascular growth influence the vascular branching pattern. We treated chick embryo CAMs daily from day 7 to day 14 postfertilization with 0.9% NaCl, angiotensin II (ANG-II), ANG-II in combination with different angiotensin receptor subtype antagonists, i.e., losartan and CGP 42112A, or the prostaglandin synthesis inhibitor acetylsalicylic acid (ASA). Arcade formation was quantified by counting the number of arcades per cm2 treated area, the branch-node ratio and mean surface area of arcade loops. ANG-II caused a 2-fold increase in the number of arcades versus 0.9% NaCl. Addition of ASA or losartan caused a further enhancement of arcade formation expressed in the number and branch-node ratio. CGP 42112A had no significant effect on arcade formation. From these data we hypothesize that ANG-II stimulates the process of capillary upgrading to arterioles by stimulation of arteriolar smooth muscle cell growth. Prostaglandins normally counteract this effect. After blockade of prostaglandin action, the ANG-II-induced arterialization is enhanced, resulting in pronounced arcade formation. The actions of losartan may be related to its inhibitory effects on prostaglandins rather than angiotensin receptor antagonism.

The effects of locally applied adenosine (ADO) and/or femoral artery pressure reduction (induced by complete aorta occlusion) on capillary diameter were investigated in the tenuissimus muscle of anesthetized rabbits. Capillaries were visualized by means of intravital video microscopy. Diameters were measured using an image shearing device. During control femoral artery pressure (median: 83 mm Hg) and without ADO, median capillary diameter was 4.3 microns (range: 3.2-5.3 microns; 27 capillaries in 7 animals). Complete aorta occlusion (median femoral artery pressure: 18 mm Hg) resulted in a reduction of capillary diameter to 3.9 microns (2.7-4.7 microns; p < 0.0001). Subsequent reactive hyperemia resulted in an increase in diameter to 5.2 microns (3.7-6.0 microns; p < 0.0001). Locally applied ADO (10(-4) M) probably led to complete vasodilation of the arterioles, because their diameters did not further increase during reactive hyperemia after complete occlusion. ADO (10(-4) M) induced an increase of control capillary diameter to 5.5 microns (4.1-6.4 microns; median relative increase: 27%; p < 0.0001), resulting in a decrease of capillary resistance by 61%. In the presence of ADO, aorta occlusion resulted in a capillary diameter decrease to 4.7 microns (3.4-6.1 microns); p < 0.0001). Subsequent reactive hyperemia resulted in an increase to maximally 5.6 microns (4.3-6.4 microns; p < 0.0001). This diameter was approximately the same as the control diameter during ADO. During occlusion in the presence of ADO, capillary diameter was significantly larger (11%; p < 0.0001) than during control without ADO. The capillary diameter changes induced by the various interventions were mainly passive, i.e., proportional to capillary transmural pressure changes. However, capillary diameter was larger during aortal occlusion in the presence of ADO than during control femoral artery pressures without ADO, even though capillary pressure was probably higher in the latter case. It is proposed that the prolonged increase in transmural capillary pressure due to ADO may induce changes in capillary wall configuration, leading to larger diameters.