In Angiotensin II-induced hypertension, maintained nitric oxide production in afferent arterioles counteracts the enhanced afferent arteriolar reactivity to Angiotensin II.
The present study was conducted to determine the contribution of nitric oxide to angiotensin II (Ang II) reactivity of afferent and efferent arterioles from Ang II-infused hypertensive rats. Experiments were performed in vitro with the blood-perfused juxtamedullary nephron technique 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 arteriolar diameter (18.1+/-0.6 microm; n=12) by 10.0+/-0.7%, 28.1+/-1.7%, and 52.8+/-1.9%, respectively, and efferent arteriolar diameter (17.2+/-1.4 microm; n=8) decreased by 9.3+/-0.7%, 27.0+/-1.2%, and 50.4+/-1.6%, respectively. Nitric oxide synthase inhibition with 100 micromol/L N(omega)-nitro-L-arginine (NLA) reduced resting afferent and efferent arteriolar diameters to 14.7+/-0.4 and 14.3+/-1.2 microm, respectively, and enhanced afferent but not efferent arteriolar reactivity to Ang II. The enhanced afferent arteriolar reactivity to Ang II was eliminated by addition of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP, 10 micromol/L), which reversed the NLA-induced decrease in diameter. Addition of 10 micromol/L SNAP, without NLA, blunted efferent but not afferent arteriolar reactivity to Ang II. Afferent (n=7) and efferent arteriolar diameters (n=6) decreased by 48.5+/-2.2% and 41.0+/-1.9%, respectively, in response to 10 nmol/L Ang II. These results suggest that in this model of hypertension, maintained nitric oxide production in afferent arterioles counteracts the enhanced afferent arteriolar reactivity that occurs in Ang II-induced hypertension.
Ichihara et al. (1998) studied this question.