1. Evidence indicates that nitric oxide (NO) exerts a paracrine influence in the renal medulla. Increases in papillary blood flow are thought to be an important determinant of the renal response to extracellular volume expansion. Therefore, in the present study, we have evaluated the role of NO in mediating papillary blood flow (laser-Doppler flowmetry) and excretory responses to volume expansion with isotonic saline (3% body weight, 15 min).
2. Infusion of the NO synthesis inhibitor Nω-nitro-l-arginine methyl ester (10 μg min−1 kg−1), significantly attentuated the renal diuretic and natriuretic responses to volume expansion as well as the renal hydrostatic interstitial pressure increase induced by this manoeuvre. The percentages of the water and sodium excreted in 1 h by the Nω-nitro-l-arginine methyl ester-pretreated animals were 36% and 40% of the load, whereas those of the control animals were 44% and 65%, respectively.
3. In similar experiments performed in the exposed papilla of Munich Wistar rats, the same dose of Nω-nitro-l-arginine methyl ester reduced basal papillary blood flow and blunted the elevation in papillary blood flow induced by volume expansion (6% versus 16% in the control animals).
4. These results indicate that the inhibition of NO synthesis blunts the renal excretory and papillary responses to volume expansion, suggesting that NO modulates these responses through changes in papillary blood flow and renal interstitial hydrostatic pressure.
