The complexity of the signal transduction pathways linked to α 1A-adrenoceptors are becoming clearer. At one time it was thought that the α 1A-subtype was linked to the influx of extracellular Ca 2+ while the α 1B-subtype was linked via inositol phosphate formation to the release of intracellular Ca 2. However the coupling of the α 1-adrenoceptors to G-proteins leads to the activation of a number of different effector enzymes which produce intracellular second messengers and alterations in biological activity. One area of diversity is in the many forms of the Gα, β, γ heterotrimeric G-proteins which confer specificity towards certain effectors. All α 1-adrenoceptor subtypes have been shown to couple to phospholipase C in many cells and tissues leading to the breakdown of PiP 2 to give IP 3, which releases intracellular Ca 2+, and diacylglycerol, which stimulates protein kinase C. Additional effectors which can couple to α 1-adrenoceptors include phospholipase D, adenylate cyclase and the mitogen-activated protein kinase pathway. The latter involves a longer term response and causes increased cell growth and may be important in, for example, the prostate as well as in vascular smooth muscle and the heart. In human prostate α 1-adrenoceptor activation leads to the release of intracellular Ca 2+ from ryanodine-sensitive store followed by an influx of extracellular Ca 2+, a mechanism different from that linked to the same receptor subtype in several other smooth muscles. Therefore a given α 1-subtype may be coupled to a variety of different signal transduction mechanisms in different systems. Further, there may be different effector mechanisms linked to α 1-subtypes in a given cell or tissue eg phospholipase C and mitogen-activated protein kinase. An increased understanding of the complexity of signal transduction mechanisms and the elucidation of the details in a particular tissue will open up new possibilities for therapeutic interventions.