Tubuloglomerular feedback is an intrarenal control mechanism designed to regulate the amount of salt entering the distal nephron. Its regulatory efficiency depends upon the magnitude of the vascular response to changes in the luminal signal (the feedback relationship) and on the adjustments in proximal absorption, which determine the macula densa signal (the feedforward relationship). Studies of the feedback relationship have established that the vascular response is related to macula densa solute concentration in a sigmoidal fashion, with the normal operating point located somewhere in the steep portion of the curve. Thus, tubuloglomerular feedback tonically suppresses glomerular filtration rate, an effect that may be even more pronounced in juxtamedullary nephrons. An alteration in the feedforward function and thus in the macula densa signal is likely to participate in the vascular resistance changes initiated by changes in arterial pressure, elevated protein intake, or ADH administration. Our understanding of the intra- and intercellular mechanisms underlying information transfer across the JGA is currently incomplete, but there is some information about the biochemical characteristics of the cellular components. The enzymatic and surface properties establish the distinct nature of the macula densa cells and indicate a distinct function.