Increased intracellular pH at the macula densa activates nNOS during tubuloglomerular feedback

摘要: Increased intracellular pH at the macula densa activates nNOS during tubuloglomerular feedback. Background The senses increasing NaCl concentrations in tubular fluid and increases afferent arteriole tone by a process known as feedback (TGF). Nitric oxide (NO) production neuronal nitric synthase (nNOS) is enhanced lumen, NO thus formed inhibits TGF. Blocking apical Na + /H exchange with amiloride augments TGF mimics effect of inhibition. We hypothesized that lumen raises (pH i ) nNOS. Methods thick ascending limb portion distal tubule intact plaque adherent to glomerulus were microdissected perfused. Macula perfusate was changed from low (10 mmol/L) high solution (80 mimic conditions induce Osmolality both solutions 180 mOsm, so changing did not alter cell volume. Results increased significantly 7.0 ± 0.5 7.8 0.6 when ( P N = 5). When added inhibit exchange, increase blocked Fluorescence intensity DAF-2, an NO-sensitive dye, 28.8 4.1% after luminal 5), indicating production. In presence exchanger inhibitor or 7-NI, induced switching blunted. To study whether changes can directly production, we used nigericin, K ionophore, equilibrate pH. raised 7.3 10 −5 mol/L nigericin solution, fluorescence DAF-2 17.9 1.3% raising Conclusion concluded TGF, this nNos.