Abstract
Brain, or type I, nitric oxide synthase is expressed strongly in the macula densa of the kidney. Functional studies show that it blunts the tubuloglomerular feedback response that causes vasoconstriction of the renal afferent arteriole in response to sodium chloride reabsorption at this site, and regulates renin release from the juxtaglomerular apparatus. Studies published this year have made great progress in defining the mechanism of action of type I nitric oxide synthase on tubuloglomerular feedback. Macula densa-derived nitric oxide can act via both the autocrine and probably the paracrine routes. Nitric oxide bioactivity in the juxtaglomerular apparatus is strongly curtailed by oxidative stress in hypertensive models. The signalling pathways within macula densa cells have been examined in detail. Nitric oxide synthase type I in the macula densa probably adapts renal hemodynamics and possibly renin secretion to changes in blood pressure and salt intake.
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