Determinants of renal vasoconstriction after systemic inhibition of nitric oxide synthesis in rats.

Abstract

The effects of NG-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) on renal hemodynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abdominal aorta, and rats in which tubuloglomerular feedback was inhibited by furosemide pretreatment, ureteral ligation, or both interventions combined. In control rats, L-NNA increased (P < 0.05) renal vascular resistance (274 +/- 27%) along with systemic arterial (54 +/- 4%) and renal perfusion (54 +/- 5%) pressures and decreased (P < 0.05) renal blood flow (57 +/- 4%). In rats in which renal perfusion pressure was prevented from increasing along with systemic arterial pressure (54 +/- 4%), the L-NNA-induced elevation of renal vascular resistance (173 +/- 27%) was less intense (P < 0.05). In another study, where renal perfusion pressure was fixed at pre-L-NNA levels, L-NNA-induced increases in renal vascular resistance (130 +/- 20%) were attenuated (P < 0.05) further with furosemide pretreatment (52 +/- 12%), with ureteral ligation (75 +/- 10%), and with furosemide pretreatment and ureteral ligation combined (32 +/- 8%). These data suggest that vasoconstrictor mechanisms linked to tubuloglomerular feedback and perfusion pressure elevation contribute to renal vasoconstriction after systemic inhibition of nitric oxide synthesis with L-NNA.