Glomerular immune injury in the rat: The influence of angiotensin II and α-adrenergic inhibitors

Glomerular immune injury in the rat: The influence of angiotensin II and a-adrenergic inhibitors. Nephron filtration rate (SNGFR) decreases significantly after the administration of large doses of antiglomerular basement membrane antibody (anti-GBM) as a result of reductions in both nephron (renal) plasma flow (RPF) and the glomerular permeability coefficient (LA). We have examined the participation of angiotensin II (All) and c-adrenergic activity in this process in paired studies in three groups of Munich-Wistar rats: group I, control and untreated; group 2, rats receiving continuous infusion of sar'-ala8-AI1 (1 i.g kg of body wt' min'), an All receptor antagonist; and group 3, rats receiving continuous infusion of phentolamine (27 ig . kg body wt' min), a dose sufficient to block ct-adrenergic responses. In group I, SNGFR decreased from 58 4 to 35 6 nI min' g kidney wt '(P < 0.001) after anti-GBM administration due to reductions in RPF (272 35tol70±52nl.min.gofkidneywu',P<o.oool)andLA(o.l3± 0.03 to 0.04 0.01 nl sec' g of kidney wt mm Hg', P <0.02). In group 2, the sar'-ala8-Al I-infused rats, SNGFR decreased to a greater extent than it did in group 1 (P < 0.0l)(55 2 to 18 6nI . min' gof kidney wF', P <0.005) due to a greater reduction in RPF and a similar decrease in LA. In group 3, phentolamine infusion prevented the decrease in SNGFR (52 3 to 52 4 nI min' g of kidney wt', NS) due primarily to elimination of vasoconstriction and a significantly lesser reduction in LA (0.10 0.02 to 0.07 0.01 nI sec g of kidney wt mm Hg'). There were no morphologic differences after anti-GBM administration that were unique to group 3. Blockade of All activity does not prevent immune induced vasoconstriction or the reduction in LA. ci-Adrenergic blockade (1) prevents acute immune induced vasoconstriction and (2) partially prevents the immune induced reduction in LA.