Influence of NaCl Concentration at the Macula Densa on Angiotensin II–Induced Constriction of the Afferent Arteriole

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Abstract
The macula densa, a plaque of specialized tubular epithelial cells, monitors NaCl concentrations in tubular fluid and controls resistance of the glomerular afferent arteriole (AA). In vivo micropuncture studies suggest that there are significant interactions between angiotensin II (Ang II) and macula densa control of glomerular hemodynamics. We tested the hypothesis that Ang II causes stronger constriction of the AA when NaCl concentration at the macula densa is elevated. Rabbit AAs and the attached macula densa were simultaneously microperfused in vitro, and dose-response curves to Ang II were obtained when the macula densa was not perfused or was perfused with either low NaCl (Na + , 26 mEq/L; Cl − , 7 mEq/L) or high NaCl (Na + , 84 mEq/L; Cl − , 65 mEq/L). Ang II induced stronger constriction when the macula densa was perfused with high NaCl; the decrease in diameter at 100 pmol/L was 29±5.6% (n=7) compared with 2.1±1.2% (n=8) for the nonperfused macula densa or 6.1±4.2% (n=7) for low NaCl ( P <.002). However, there was no such difference in the action of norepinephrine. Adding furosemide (10 μmol/L) to the macula densa perfusate abolished the difference in Ang II action between low and high NaCl at the macula densa. Since AA tone is higher when the NaCl concentration at the macula densa is elevated, we tested whether augmented Ang II action is due to higher AA tone. Preconstriction of the AA by 20% with norepinephrine had no effect on Ang II action. Thus, our results demonstrate that sensitivity of the AA to Ang II increases when NaCl concentration at the macula densa is elevated. Such modulation of Ang II action by macula densa NaCl concentration may be important in the control of glomerular hemodynamics.