Angiotensin II release from rabbit intrarenal arteries: a critical assessment

A microdissected rabbit intrarenal arterial network (IAN) perfused at constant flow with Krebs-bicarbonate solution was employed to determine whether this network, which has a high renin content, releases angiotensin II (AII) either spontaneously or during beta-adrenergic stimulation. Six groups of experiments were conducted in which samples of the vascular effluent were collected on Sep Paks before and during intraluminal infusion of L-isoproterenol (1.1 to 11 microg/min). Separation and assay of AII were by combined HPLC and RIA. For an accurate estimation of the quantity of AII released, it was important to subtract the Krebs and isoproterenol blanks, 19 and 23 pg, respectively, from the basal and isoproterenol-induced AII release. In Groups 1 and 2, AII release was determined before and during isoproterenol infusion (5.5 microg/min). Basal release of AII was insignificant in Groups 1 to 5. In Group 1, infusion of isoproterenol caused AII release from IAN before and after removal of glomeruli (glomerulectomy), but with variability between experiments. An even higher infusion rate of isoproterenol (11 microg/min) in Group 2 caused no significant AII release. Similarly, in Group 3, in which a longer collection period was imposed, isoproterenol (5.5 microg/min) failed to cause significant AII release. In Groups 4 and 5, Goldblatt hypertensive and salt-restricted rabbits, respectively, isoproterenol caused AII release, but the effect was statistically significant only in Group 4. Supplying renin substrate in Group 6 caused only a small spontaneous AII release. We conclude that under these conditions of complete isolation from the intact circulation, the IAN despite a high renin content, releases little locally generated AII.