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 determin e whether this network, which has a high renin content, releases angio tensin II (AII) either spontaneously or during beta-adrenergic stimula tion. Six groups of experiments were conducted in which samples of the vascular effluent were collected on Sep Paks before and during intral uminal infusion of L-isoproterenol (1.1 to 11 mu g/min). Separation an d assay of AII were by combined HPLC and RIA. For an accurate estimati on of the quantity of AII released, it was important to subtract the K rebs and isoproterenol blanks, 19 and 23 pg, respectively, from the ba sal and isoproterenol-induced AII release. In Groups 1 and 2, AII rele ase was determined before and during isoproterenol infusion (5.5 mu g/ min). Basal release of AII was insignificant in Groups 1 to 5. In Grou p 1, infusion of isoproterenol caused AII release from IAN before and after removal of glomeruli (glomerulectomy), but with variability betw een experiments. An even higher infusion rate of isoproterenol (11 mu g/min) in Group 2 caused no significant AII release. Similarly, in Gro up 3, in which a longer collection period was imposed, isoproterenol ( 5.5 mu g/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 sig nificant only in Group 4. Supplying renin substrate in Group 6 caused only a small spontaneous AII release. We conclude that under these con ditions of complete isolation from the intact circulation, the IAN des pite a high renin content, releases little locally generated AII. (C) 1997 American Journal of Hypertension, Ltd.