INTERACTIVE NITRIC-OXIDE ANGIOTENSIN-II INFLUENCES ON RENAL MICROCIRCULATION IN ANGIOTENSIN-II-INDUCED HYPERTENSION

The present study was conducted to determine the contribution of nitri c oxide to angiotensin II (Ang II) reactivity of afferent and efferent arterioles from Ang II-infused hypertensive rats. Experiments were pe rformed in vitro with the blood-perfused juxtamedullary nephron techni que in kidneys harvested from hypertensive Sprague-Dawley rats (181+/- 1 mm Hg) that had received 60 ng/min Ang II subcutaneously for 13 days . Superfusion with 0.1, 1, and 10 nmol/L Ang II reduced afferent arter iolar diameter (18.1+/-0.6 mu m; n=12) by 10.0+/-0.7%, 28.1+/-1.7%, an d 52.8+/-1.9%, respectively, and efferent arteriolar diameter (17.2+/- 1.4 mu m; n=8) decreased by 9.3+/-0.7%, 27.0+/-1.2%, and 50.4+/-1.6%, respectively. Nitric oxide synthase inhibition with 100 mu mol/L N-ome ga-nitro-L-arginine (NLA) reduced resting afferent and efferent arteri olar diameters to 14.7+/-0.4 and 14.3+/-1.2 mu m, respectively, and en hanced afferent but not efferent arteriolar reactivity to Ang II. The enhanced afferent arteriolar reactivity to Ang IT was eliminated by ad dition of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP , 10 mu mol/L), which reversed the NLA-induced decrease in diameter. A ddition of 10 mu mol/L SNAP, without NLA, blunted efferent but not aff erent arteriolar reactivity to Ang II. Afferent (n=7) and efferent art eriolar diameters (n=6) decreased by 48.5+/-2.2% and 41.0+/-1.9%, resp ectively, in response to 10 nmol/L Ang II. These results suggest that in this model of hypertension, maintained nitric oxide production in a fferent arterioles counteracts the enhanced afferent arteriolar reacti vity that occurs in Ang II-induced hypertension.