A Critical Assessment

A microdissected rabbit intrarenal arterial glomeruli (glomerulectomy) , but with variability between experiments. An even higher infusion network (IAN) perfused at constant flow with rate of isoproterenol (11 mg/min) in Group 2 Krebs-bicarbonate solution was employed to caused no significant AII release. Similarly, in determine whether this network, which has a high Group 3, in which a longer collection period was renin content, releases angiotensin II (AII) either imposed, isoproterenol (5.5 mg/min) failed to spontaneously or during b-adrenergic stimulation. cause significant AII release. In Groups 4 and 5, Six groups of experiments were conducted in Goldblatt hypertensive and salt-restricted rabbits, which samples of the vascular effluent were respectively, isoproterenol caused AII release, but collected on Sep Paks before and during the effect was statistically significant only in intraluminal infusion of L-isoproterenol (1.1 to 11 Group 4. Supplying renin substrate in Group 6 mg/min) . Separation and assay of AII were by caused only a small spontaneous AII release. We combined HPLC and RIA. For an accurate conclude that under these conditions of complete estimation of the quantity of AII released, it was isolation from the intact circulation, the IAN important to subtract the Krebs and isoproterenol despite a high renin content, releases little locally blanks, 19 and 23 pg, respectively, from the basal generated AII. q 1997 American Journal of and isoproterenol-induced AII release. In Groups Hypertension, Ltd. Am J Hypertens 1997;10:306– 1 and 2, AII release was determined before and 314 during isoproterenol infusion (5.5 mg/min) . Basal release of AII was insignificant in Groups 1 to 5.