We have studied the effects of 1-heptanol and nifedipine on noradrenaline (NA)-induced contractions in order to explore the role of gap junctions and their interactions with L-type Ca²⁺ channel mediated [Ca²⁺]o entry in the generation of NA-induced contractions in the rat vas deferens. Application of 20 μM NA to rat vas deferens resulted in contractions with three different components, an initial phasic component followed by a tonic component overlapped with an oscillatory component. Heptanol (0.01-2 mM) induced a concentration dependent reduction of the contractions. 2 mM heptanol reduced the phasic component by 32.9 ± 4.4% and the tonic component by 93.8 ± 1.9% of control, while the oscillatory component was completely abolished (n=7). Nifedipine (2 μM) reduced the phasic component by 34.5 ± 4.1% and the tonic component by 89.5 ± 3.8% of control and abolished the oscillatory component (n=6). In the presence of heptanol and nifedipine together, the phasic component was reduced by 61.3 ± 8.3% and the tonic component by 94.5 ± 1.0% of control. The oscillatory component was completely abolished (n=6). These results allow the conclusion that phasic contraction is mainly due to the direct action of NA, independent of gap junctions, while the tonic and oscillatory contractions may depend significantly on cell-to-cell communication. These in turn may depend critically on the availability of extracellularly derived Ca²⁺.