The effects of ryanodine, cyclopiazonic acid (CPA), and nifedipine on noradrenaline (NA)-induced contractions were investigated to characterize the role of the sarcoplasmic reticulum (SR) in the epididymal and prostatic parts of the rat vas deferens. In the epididymal part, NA (0.1, 1, and 100 microM) evoked marked rhythmic contractions superimposed on a tonic response. NA (100 microM) evoked biphasic tonic contractions consisting of a fast (initial) component and delayed secondary components. Nifedipine (1 microM) suppressed the rhythmic activity and the contractions to low NA concentrations and markedly reduced the components of the response to NA (100 microM). Contractions of the epididymal part to NA (0.1, 1, and 100 microM) were not blocked by ryanodine (1-30 microM) or CPA (1-30 microM). The secondary component in the response to NA (100 microM) was enhanced by CPA (> or =10 microM). Thus in the epididymal part, NA stimulates contraction predominantly by mobilizing extracellular calcium. However, a residual nifedipine-insensitive contraction to NA (100 microM) was observed and was not blocked by ryanodine (30 microM) or CPA (30 microM). In the prostatic part, NA evoked mainly tonic contractions. The response to NA (100 microM) consisted of three distinct components. Nifedipine (1 microM) reduced the contractions to low concentrations of NA (0.1 and 1 microM) and all three components of the response to NA (100 microM). Contractions of the prostatic part to low concentrations of NA (0.1 and 1 microM) were not blocked by CPA (30 microM) or ryanodine (30 microM). The components of the response to NA (100 microM) were affected differently by the drugs. Ryanodine (17-30 microM) or CPA (1-30 microM) suppressed the initial component and reduced the second component. The third component was largely unaffected by CPA but reduced by ryanodine. In the additional presence of nifedipine (1 microM), the residual components of NA (100 microM) response were markedly reduced and the contractions to low concentrations of the agonist virtually abolished. These results suggest that NA contracts the prostatic part by mobilizing both extra- and intracellular calcium. These results show that NA-induced contractions of the epididymal and prostatic parts of the rat vas deferens differ in sensitivity to ryanodine or CPA. The results suggest that, during stimulation of the epididymal part, the SR functions mainly to buffer calcium entering through nifedipine-sensitive voltage-gated calcium channels. In contrast, in the prostatic part, the SR serves mainly as a source of calcium and contributes more to contractions evoked by higher concentrations of the agonist.