Macula densa nitric oxide synthase: Expression, regulation, and function  Christopher S. Wilcox, William J. Welch  Kidney International  Volume 54, Pages S53-S57 (September 1998) DOI: 10.1046/j.1523-1755.1998.06711.x Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 1 Percentage changes in maximal tubuloglomerular feedback (TGF) responses of nephrons from rats adapted to low (A) or high (B) salt intakes during orthograde perfusion of the loop of Henle at 40 nl/min with artificial tubular fluid (ATF) containing l-arginine (10-3 M), l-lysine (2 × 10-3 M), or l-homoarginine (2 × 10-3 M), singly or together. Means ± sem. ** P < 0.01 versus ATF + vehicle. Kidney International 1998 54, S53-S57DOI: (10.1046/j.1523-1755.1998.06711.x) Copyright © 1998 International Society of Nephrology Terms and Conditions

Figure 2 Cell diagram showing hypotheses for regulation of macula densa cell brain nitric oxide synthase (bNOS). Solute absorption via an Na+/K+/2Cl, furosemide-inhibitable luminal cotransporter activates bNOS, perhaps via increases in intracellular calcium concentration. l-Arginine uptake into the cell via system y+ is inhibited by l-ornithine, l-lysine, and l-homoarginine and by symmetric and asymmetric dimethylarginine (SDMA and ADMA) and monomethyl l-arginine (L-NMA). ADMA and L-NMA also inhibit bNOS activity. NO generated in the macula densa cell is degraded by interaction with oxygen radicals (O2-) to peroxynitrite (ONOO-). Kidney International 1998 54, S53-S57DOI: (10.1046/j.1523-1755.1998.06711.x) Copyright © 1998 International Society of Nephrology Terms and Conditions