Tubuloglomerular feedback (TGF) and the myogenic mechanism control afferent arteriolar diameter in each nephron and regulate blood flow. Each mechanism generates a self-sustained oscillation, the oscillations interact, TGF modulates the frequency and amplitude of the myogenic oscillation, and the oscillations synchronize; a frequency ratio of 5:1 is the most frequent. TGF oscillations synchronize in nephron pairs supplied from a common cortical radial artery. Myogenic oscillations also synchronize. We hypothesize that electrotonic vascular signal propagation from one juxtaglomerular apparatus interacts with similar signals from other nephrons to produce synchronization. We tested this idea in tubular-vascular preparations from mice. Vascular smooth muscle cells were loaded with a fluorescent voltage sensitive dye; fluorescence intensity was measured with confocal microscopy. Perfusion of the thick ascending limb activated TGF and depolarized afferent arteriolar smooth muscle cells. The depolarization spread to the cortical radial artery and other afferent arterioles, and declined with distance from the perfused juxtaglomerular apparatus, consistent with electrotonic vascular signal propagation. With a mathematical model of 2 coupled nephrons we estimated the conductance nephron coupling by fitting simulated vessel diameters to experimental data. With this value we simulated nephron pairs to test for synchronization. In single nephron simulations the frequency of the TGF oscillation varied with nephron length. Coupling nephrons of different lengths forced TGF frequencies of both members of the pair to converge to a common value. The myogenic oscillations also synchronized. The result confirms that electronic vascular signal propagation is a plausible mechanism for nephron synchronization. Coupling increased the stability of the various oscillations.