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

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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 (K(f)) 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 μl min-1 and 5 ± 2 to 342 ± 12 μmol 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 K(f). The results suggest that NO may play an important role in the regulation of renal haemodynamics and glomerular function.

Original languageEnglish
Pages (from-to)159-167
Number of pages9
JournalThe Journal of Physiology
Volume475
Issue number1
Publication statusPublished - 1994
Externally publishedYes

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