In rats peristaltic activity of the upper urinary tract is generated in the proximal renal pelvis. It inserts deep in the renal parenchyma and may be exposed to the high renal endothelin-1 (ET-1) concentrations. Renal pelvic ET_A receptor expression increases with dietary NaCl restriction. We tested the hypotheses that ET-1 stimulates renal pelvic peristalsis and that the sensitivity of renal pelvic peristalsis to stimulation with ET-1 increases with dietary NaCl restriction. Peristaltic activity of isolated rat renal pelvises was investigated by wire myography. To test the effect of differential NaCl intake on pelvic peristalsis, rats were fed NaCl-deficient or high (1.8%) NaCl diets 2 weeks prior to the studies on isolated renal pelvises. ET-1 increased peristaltic activity of renal pelvises by 300% of basal peristaltic activity in a concentration-dependent manner. This was due to both increased frequency and amplitude of peristaltic waves. ET_A receptor blockade but not ET_B receptor blockade potently inhibited ET-1-induced activation of pelvic peristalsis. Cyclooxygenase (COX) 1 but not COX 2 inhibition blunted the ET-1-induced activation of pelvic peristalsis. Nonselective Rho kinase (ROCK) inhibition reduced spontaneous pelvic peristaltic activity to 20% of basal activity. During ROCK inhibition, ET-1 concentration-dependently stimulated pelvic peristalsis but peristaltic activity remained at 20% of corresponding responses without ROCK inhibition. Western-blot analyses did not show increased phosphorylation of ROCK substrates in isolated ET-1-treated renal pelvises. Differential NaCl intake did not affect basal and ET-1-stimulated pelvic peristalsis. ET-1 is a powerful ET_A receptor-dependent activator of renal pelvic peristalsis and COX1 products are important mediators of this effect. ROCK activity strongly determines basal pelvic peristaltic activity but appears less important for mediating the stimulatory ET-1 effects. ET-1 could play an important role for the paracrine regulation of renal pelvic peristalsis.