Atrial natriuretic factor inhibits hypertonic saline-mediated decreases in renal hemodynamics

The present study in the anesthetized dogs was designed to test the hypothesis that atrial natriuretic factor (ANF) attenuates whole kidney tubuloglomerular feedback (TGF) mediated decreases in renal blood flow (RBF) and glomerular filtration rate (GFR) produced by hypertonic saline (HS). Secondly, as adenosine (AD) has been implicated as a metabolic mediator of TGF, we also hypothesized that ANF would antagonize the renal actions of AD. To test this hypothesis, RBF and GFR were assessed in response to hypertonic saline (HS, 16%, i.r.) or adenosine (AD, 0.1 μmol/min, i.r.) in the presence and absence of exogenous ANF (100 ng/kg/min, i.r.). ANF attenuated HS-mediated reductions in GFR (HS, -39.6 ± 9.8 ml/min vs. HS + ANF, -14.3 ± 4.5 ml/min, P < 0.05) and in RBF (HS, -143 ± 35 ml/min vs. HS + ANF, -5 ± 22 ml/min, P < 0.05). GFR was reduced by AD (-9.2 ± 3.0 ml/min, P < 0.05), but maintained by AD + ANF (-0.4 ± 2.0 ml/min, NS). A transient adenosine-mediated vasoconstriction was attenuated by ANF (AD, -54.5 ± 3.6 ml/min vs. AD + ANF, -3.7 ± 3.1 ml/min, P < 0.005). We conclude that ANF at pharmacologic concentrations attenuates at the whole kidney level hypertonic saline and adenosine-mediated reductions in RBF and GFR.