During urinary tract infection there is abnormal contractility of the ureters but little is known about the normal characteristics of ureteric physiology or how bacterial infection modulates smooth muscle contraction. We aimed to characterise the primary mediators controlling normal ureteric physiology using pharmacological tools and biochemical methods. Phasic contractions and calcium transients evoked by electrical field stimulation (EFS) of rings of human ureter loaded with the ratiometric calcium indicator Indo-1 were studied. Exposure to pharmacological agents which modulate L-type calcium channels (1μM BayK8644 and 10μM Nifedipine), SERCA pump (20μM CPA) and BK_Ca channels (1mM TEA) was performed by perfusing the tissue rings at 35^οC with each drug. Further to this we studied the expression and tissue distribution of SERCA 1-3, BK_Ca α and β , RyR 1-3, L-type calcium channels and IP₃R in human ureters. Tissues were obtained with informed consent from healthy renal transplant live-donors and studied using western blotting and immunohistochemical tissue microarray techniques with a panel of well characterized isoform specific antibodies. BayK8644 produced a time-dependent increase in the amplitude and duration of both calcium transients and phasic contractions while nifedipine caused their inhibition. TEA at 1mM, which blocks mainly BK_Ca channels produced an increase in the amplitude and duration of the calcium transients and phasic contractions, implicating the involvement of BK_Ca channels in controlling contraction. On increasing the dose to 10mM it produced a further increase suggesting the involvement of K_v channels. Inhibition of the SERCA with CPA produced only a small increase in the amplitude of calcium transients and phasic contractions. Biochemical and immunohistochemical studies showed that the human ureter expresses 2 isoforms of SERCA (2 and 3), L type calcium channels and BK_Ca α and β in the smooth muscle while RyR3 and IP₃R are expressed in the smooth muscle and urothelium. These studies show for the first time that it is possible to measure force stimulated by electrical field stimulation (EFS) while simultaneously recording emitted signals from the dual emission calcium indicator Indo-1 AM in cross-sectional rings of human ureter. Studies also show that contraction of the human ureter is regulated in part by L-type calcium channels and BK_Ca channels. Compared to other phasic smooth muscles the role sarcoplasmic reticulum appears to be small. Current work is establishing how infection interferes with the Ca signalling.