It is a consistent anatomical feature of all mammalian and many vertebrate kidneys that a segment of the distal tubule is firmly attached to the vascular pole of its own glomerulum. In mammalian kidneys, the tubular epithelium at the point of contact is differentiated into a specialized plaque of cells called the macula densa (MD). The MD cells together with underlying interstitial cells and glomerular arteriolar smooth muscle cells form the juxtaglomerular apparatus (JGA). The JGA also contains the juxtaglomerular granular cells, modified smooth muscle cells responsible for synthesis, storage, and secretion of renin. The juxtaglomerular connection between tubule and glomerular arterioles is the structural basis of a functional interaction called tubuloglomerular feedback, TGF (The Kidney Physiology and Pathophysiology, Lippincott Williams & Wilkins 945-980, 2000). Whenever NaCl concentration at the macula densa is perturbed by changes in GFR or in fluid absorption along the proximal nephron, a signaling cascade is initiated that results in a dilatation of afferent arterioles when MD NaCl concentration decreases, and a constriction when MD NaCl concentration increases. Dilatation and constriction of afferent arterioles is associated with increases or decreases of single nephron glomerular filtration rate (SNGFR) respectively, and these changes tend to return MD NaCl towards normal. A second mechanism that affects distal NaCl concentration is the mechanism of glomerulotubular balance (GTB), the direct relationship between tubular flow and tubular fluid reabsorption. Thus, by stabilizing distal NaCl concentration, TGF and GTB contribute to the stabilization of NaCl excretion.
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