The intrarenal tubuloglomerular feedback mechanism operates at the site of contact between the thick ascending limb and glomerulus where specialized macula densa cells detect changes in tubular fluid composition and transmit information to the smooth muscle cells of the afferent arteriole. Increases in tubular fluid osmolality result in the transmission of vasoconstrictor signals and decreases in the rate of filtrate formation. Recent studies have identified two sites at which cytosolic calcium may play important roles. First, studies indicate that tubuloglomerular mediated vasoconstriction involves calcium mediated excitation contraction coupling of smooth muscle cells of the afferent arteriole. This calcium mediated event is sensitive to calcium channel blockade. Second, recent studies suggest that the macula densa cells may detect changes in tubular fluid osmolality through a cytosolic calcium system. The use of intracellular calcium antagonists further suggests that intracellular calcium mobilization is the primary mechanism responsible for increases in macula densa cytosolic calcium with increases in tubular fluid osmolality. Calmodulin and cyclic AMP may serve as modulators of this cytosolic calcium system. These studies suggest that calcium plays important roles in the regulation of renal hemodynamics.