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Abstract: It has been postulated that in blood vessels under α1-related stimulation, the endothelial intracellular calcium concentration ([Ca2+] i ) increases, which is necessary to induce nitric oxide synthesis, is the result of an increase in vascular smooth muscle, which subsequently, flows into the endothelial cells through gap junctions and it is not the result of a direct adrenergic stimulation of endothelial receptors. Others, however, postulate that endothelial α1D-adrenoceptors, have a direct effect on nitric oxide synthesis. In order to clarify this phenomena, in this work we analyzed the presence of α1receptor subtypes and their functional association with nitric oxide synthesis in rat coronary microvascular endothelial cells in culture, with pharmacological, immunological and reverse transcriptase polymerase chain reaction approaches. Our results show the presence and functional coupling with nitric oxide synthesis of α1A and α1D-adrenoceptor subtypes. α1B-adrenoceptor subtype is not coupled with nitric oxide production. [Copyright &y& Elsevier]