The a-antagonism produced by prazosin and the other quinazoline derivatives is of the equilibrium-competitive type. The drugs are selective for a1-adrenoceptors, so that at usual therapeutic concentrations there is little or negligible antagonism of a2-adrenoceptors. However, selectivity is only relative and can be lost with high drug concentrations. While most of the pharmacological effects of prazosin are directly attributable to a1-antago-nism, at high doses the drug can cause vasodilation by a direct effect on smooth muscle independent of a-recep-tors. This action appears to be related to an inhibition of phosphodiesterases that results in an enhancement of intracellular levels of cyclic nucleotides.
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