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 α 1-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 α 1-adrenoceptor antagonist prazosin (10 − 7 M) was more effective than the selective α 2-adrenoceptor antagonist idazoxan (10 − 7 M) to inhibit contractions induced by electrical field stimulation, pointing out a major involvement of α 1-adrenoceptor. When noradrenaline was used instead of electrical field stimulation, it showed a high potency (pD 2 = 7.9). Noradrenaline-induced contractions were competitively blocked by the selective α 1A-adrenoceptor antagonists WB 4101 (pA 2 = 8.88), phentolamine (pA 2 = 8.39) and by the α 1B-adrenoceptor antagonist spiperone (pA 2 = 8.57), indicating the presence of functional α 1A- and α 1B-adrenoceptors. In addition, contractions were not blocked by the selective α 1D-adrenoceptor antagonist BMY 7378 (up to 10 − 6 M), while selective α 2-adrenoceptor antagonists showed low pA 2 values (yohimbine, 7.25 and idazoxan, 7.49), suggesting a minor role, if any, for α 1D- and α 2-adrenoceptors. To check the proportionate role of α 1A- and α 1B-adrenoceptors, we blocked α 1B-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 α 1B-adrenoceptor, and was inhibited by 5-methyl-urapidil (pA 2 = 8.94) and by the Ca 2+ channel blocker nifedipine (3 μM), confirming the involvement of α 1A-adrenoceptors. The presence of mRNA encoding α 1A- and α 1B-adrenoceptor was also shown on RT-PCR assays. Unexpectedly, α 1D-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 α 1A- and α 1B-, but not with α 1D- or α 2-adrenoceptor. The fact that the functional α 1D-adrenoceptor could not be detected in spite of the presence of the corresponding mRNA, remains to be investigated.