The rat testicular capsule is a thin tissue surrounding the testis, whose precise function is still unknown. We have studied the contractile effects of electrical field stimulation, noradrenaline, and the blockade by antagonists of adrenergic receptors, in order to characterize sympathetic neurotransmission, and adrenoceptor subtypes. In addition, reverse transcription polymerase chain reaction (RT-PCR) assays were made to check for the expression of the three known subtypes of α1-adrenoceptors. The effects of electrical field stimulation (2 to 20 Hz, 1 ms, 60 V) were almost totally abolished by depletion of neuronal noradrenaline storage with reserpine (10 mg/Kg), but not by the purinergic receptor antagonist suramin (10−5 M), indicating that noradrenaline, but not ATP, was involved in contractions. The selective α1-adrenoceptor antagonist prazosin (10−7 M) was more effective than the selective α2-adrenoceptor antagonist idazoxan (10−7 M) to inhibit contractions induced by electrical field stimulation, pointing out a major involvement of α1-adrenoceptor. When noradrenaline was used instead of electrical field stimulation, it showed a high potency (pD2 = 7.9). Noradrenaline-induced contractions were competitively blocked by the selective α1A-adrenoceptor antagonists WB 4101 (pA2 = 8.88), phentolamine (pA2 = 8.39) and by the α1B-adrenoceptor antagonist spiperone (pA2 = 8.57), indicating the presence of functional α1A- and α1B-adrenoceptors. In addition, contractions were not blocked by the selective α1D-adrenoceptor antagonist BMY 7378 (up to 10−6 M), while selective α2-adrenoceptor antagonists showed low pA2 values (yohimbine, 7.25 and idazoxan, 7.49), suggesting a minor role, if any, for α1D- and α2-adrenoceptors. To check the proportionate role of α1A- and α1B-adrenoceptors, we blocked α1B-adrenoceptors with chloroethylclonidine (CEC, 30 μM, 45 min), that reduced the maximal effect of noradrenaline by about 60%. The remnant CEC-insensitive noradrenaline contraction was assumed to be unrelated to α1B-adrenoceptor, and was inhibited by 5-methyl-urapidil (pA2 = 8.94) and by the Ca2+ channel blocker nifedipine (3 μM), confirming the involvement of α1A-adrenoceptors. The presence of mRNA encoding α1A- and α1B-adrenoceptor was also shown on RT-PCR assays. Unexpectedly, α1D-transcripts were also detected in these assays. Taken together, our results show that ATP co-transmission could not be detected, and that neurotransmission involves the interaction of noradrenaline with both α1A- and α1B-, but not with α1D- or α2-adrenoceptor. The fact that the functional α1D-adrenoceptor could not be detected in spite of the presence of the corresponding mRNA, remains to be investigated.