Purpose: Combination therapy of male lower urinary tract symptoms with α₁-adrenoceptor and muscarinic receptor antagonists attracts increasing interest. Propiverine is a muscarinic receptor antagonist possessing additional properties, i. e., block of L-type Ca²⁺ channels. Here, we have investigated whether propiverine and its metabolites can additionally antagonize α₁-adrenoceptors. Methods: Human prostate and porcine trigone muscle strips were used to explore inhibition of α₁-adrenoceptor-mediated contractile responses. Chinese hamster ovary (CHO) cells expressing cloned human α₁-adrenoceptors were used to determine direct interactions with the receptor in radioligand binding and intracellular Ca²⁺ elevation assays. Results: Propiverine concentration-dependently reversed contraction of human prostate pre-contracted with 10 μM phenylephrine (-log IC₅₀ [M] 4. 43 ± 0. 08). Similar inhibition was observed in porcine trigone (-log IC₅₀ 5. 01 ± 0. 05), and in additional experiments consisted mainly of reduced maximum phenylephrine responses. At concentrations ≥1 μM, the propiverine metabolite M-14 also relaxed phenylephrine pre-contracted trigone strips, whereas metabolites M-5 and M-6 were ineffective. In radioligand binding experiments, propiverine and M-14 exhibited similar affinity for the three α₁-adrenoceptor subtypes with -log K_i [M] values ranging from 4. 72 to 4. 94, whereas the M-5 and M-6 did not affect [³H]-prazosin binding. In CHO cells, propiverine inhibited α₁-adrenoceptor-mediated Ca²⁺ elevations with similar potency as radioligand binding, again mainly by reducing maximum responses. Conclusions: In contrast to other muscarinic receptor antagonists, propiverine exerts additional L-type Ca²⁺-channel blocking and α₁-adrenoceptor antagonist effects. It remains to be determined clinically, how these additional properties contribute to the clinical effects of propiverine, particularly in male voiding dysfunction.