We studied the role of angiotensin II (AII) in the interactive control of renal function by the o,-adrenergic system and nitric oxide (NO) in adult male Munich Wistar rats 5–7 days after ipsilateral renal denervation (DNX). Renal micropuncture was used under euvolemic conditions before (period l) and during (period 2) sys-temic inhibition of NO synthase (NOS) with N “"-mono-methyl-L-arginine (L-NMMA) in three groups. Group l served as a DNX control. In group 2, the o,-adrenergic agonist B-HT 933 (BHT) was infused systemically throughout the experiment. In group 3, the AII-receptor blocker, Iosartan (LOS), was infused before period 2 as well as throughout infusion of BHT. L-NMMA increased blood pressure (BP) to a similar degree in all three groups. In group 1, infusion of L-NMMA did not affect glomerular hemodynamics or tubular function. With BHT in group 2. L-NMMA reduced absolute proximal tubular reabsorption (APR) and by reducing nephron plasma flow (SNPF) and glomerular ultrafiltration coefficient (LpA) caused nephron filtration rate (SNGFR) to decrease, a response described in innervated kidneys. LOS in group 3 abrogated the BHT-facilitated reduction of LpA and SNGFR but not of SNPF and APR in response to L-NMMA. In group 1, urinary sodium excretion (UNaV) did not change and urinary flow rate (UV) increased slightly in period 2. L-NMMA combined with BHT. however, exerted a profound diuresis and natriuresis in group 2. These effects were further exaggerated with LOS. In a fourth group of DNX rats, LOS given alone before period 2 did not affect SNGFR, SNPF, LpA. APR, UV, or UNaV. We conclude that after subacute renal denervation o,-adrenergic acti-vation sensitizes (a) LpA to reduction by NOS inhibition through an AII-dependent mechanism, and (b) SNPF and proximal tubular reabsorption to reduction by L-NMMA regardless of the AII activity. Furthermore, our results suggest a potential role for the o--adrenergic system and AII in the diuretic and natriuretic effect of systemic NOS inhibition. Key Words: Micropuncture-Pressure natri-uresis–Pressure diuresis.

Systemic inhibition of nitric oxide synthase (NOS), in addition to increasing mean arterial blood pressure (BP)(1), may reduce net fluid reabsorption by the proximal tubule (APR) and nephron filtration rate (SNGFR) by causing nephron plasma flow (SNPF) and glomerular capillary ultrafiltration coefficient (LpA) to decrease (2). In a previous study, these effects of NOS inhibition on the glomerular microcirculation and proximal tubule, but not on systemic BP, were prevented by prior angiotensin II (AII) receptor blockade (2), implying that argi-