Intrarenal haemodynamic and glomerular responses to inhibition of nitric oxide formation in rabbits.

Abstract

1. The renal effects of inhibiting nitric oxide (NO) formation using N‐nitro‐L‐arginine (NOLA, 20 mg kg‐1) were examined using micropuncture techniques in pentobarbitone‐anaesthetized rabbits. 2. Renal vascular resistance doubled from 2.7 +/‐ 0.5 to 5.0 +/‐ 1.1 mmHg ml‐1 min‐1 after NOLA (P < 0.01), with similar percentage increases in both pre‐ (149 +/‐ 38%, P < 0.01) and postglomerular (158 +/‐ 42%, P < 0.01) resistance. 3. Glomerular capillary pressure rose from 33 +/‐ 1 to 40 +/‐ 1 mmHg after NOLA (P < 0.01) but despite this, glomerular filtration rate (GFR) and single nephron glomerular filtration rate did not significantly change. 4. Blood pressure increased 18 +/‐ 1 mmHg (P < 0.001) within 10 min of NOLA administration and remained near this level for the next 90 min. 5. The glomerular ultrafiltration coefficient (Kf) decreased significantly from 0.085 +/‐ 0.022 to 0.035 +/‐ 0.006 nl s‐1 mmHg‐1 (P < 0.05). 6. Urine flow and sodium excretion increased markedly (26 +/‐ 9 to 337 +/‐ 102 microliters min‐1 and 5 +/‐ 2 to 342 +/‐ 12 mumol min‐1 respectively, (P < 0.001)) and sodium fractional excretion rose from 1.0 +/‐ 0.3 to 8.0 +/‐ 2.2% (P < 0.01). 7. Thus, administration of NOLA to rabbits caused vasoconstriction of both pre‐ and postglomerular vessels, diuresis and natriuresis without significant change in GFR, and a reduction in Kf. The results suggest that NO may play an important role in the regulation of renal haemodynamics and glomerular function. © 1994 The Physiological Society