The guinea-pig ureter was placed in a three-compartment organ bath to enable the application of electrical stimuli or drugs to its renal end (R-site), the middle region (M-site) or the bladder end (B-site) while recording mechanical activity at the R- and B-sites. All experiments were performed in ureters pre-exposed to capsaicin (10 microM for 15 min) to prevent the release of sensory neuropeptides from afferent nerves. Electrical field stimulation (EFS, 5-25 ms pulse width, 20 V) produced a phasic contraction at the site of stimulation ('direct' response to EFS) which propagated to the other end of the ureter. Section of the ureter at the M-site abolished the propagated response to EFS; after section, EFS applied at the M-site induced a phasic contraction at both the R- and B-sites. Likewise, the application of KCl at the M-site produced phasic contractions at both the R- and B-sites. Tetrodotoxin (1 microM), nifedipine (1 microM) or Bay K 8644 (1 microM) applied at the M-site had no influence on the direct or propagated responses to EFS; nifedipine (10 microM) applied at the M-site abolished the propagated responses without affecting the direct responses to EFS. Bay K 8644 (1 microM) applied at the R-site produced a marked enhancement of the direct response (EFS applied at R-site) while having no effect on the amplitude of the propagated response to EFS.(ABSTRACT TRUNCATED AT 250 WORDS)