The tubuloglomerular feedback is mediated by

Signals from the renal tubule in each nephron feedback to affect filtration in its glomerulus. As the rate of flow through the ascending limb of the loop of Henle and first pa of the distal tubule increases, glomerular filtration in the same nephron decreases, and, conversely, a decrease in flow increases the GFR. This process, which is called tubuloglomerular feedback, tends to maintain the constancy of the load delivered to the distal tubule. The sensor for this response is the macula densa. The amount of fluid entering the distal tubule at the end of the thick ascending limb of the loop of Henle depends on the amount of Na+ and Cl- in it. The Na+ and Cl- enter the macula densa cells the Na-K-2Cl cotranspoer in their apical membranes. The increased Na+ causes increased Na, K ATPase activity and the resultant increased ATP hydrolysis causes more adenosine to be formed. Presumably, adenosine is secreted from the basal membrane of the cells. It acts adenosine A1 receptors on the macula densa cells to increase their release of Ca2+ to the vascular smooth muscle in the afferent aerioles. This causes afferent vasoconstriction and a resultant decrease in GFR. Presumably, a similar mechanism generates a signal that decreases renin secretion by the adjacent juxtaglomerular cells in the afferent aeriole, but this remains unsettled. Ref: Ganong&;s review of medical physiology,23rd edition,page no: 651,652