DETERMINANTS OF RENAL VASOCONSTRICTION AFTER SYSTEMIC INHIBITION OF NITRIC-OXIDE SYNTHESIS IN RATS

The effects of N-G-nitro-L-arginine (L-NNA, 10 mg/kg iv) on renal hemo dynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abd ominal aorta, and rats in which tubuloglomerular feedback. was inhibit ed by furosemide pretreatment, ureteral ligation, or both intervention s 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-indueed elevation of renal vascular resistance (173 /- 27%) was less intense (P < 0.05). In another study, where renal per fusion 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 liga tion (75 +/- 10%), and with furosemide pretreatment and ureteral ligat ion combined (32 +/- 8%). These data suggest that vasoconstrictor mech anisms linked to tubuloglomerular feedback and perfusion pressure elev ation contribute to renal vasoconstriction after systemic inhibition o f nitric oxide synthesis with L-NNA.