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Summary 1 The effects of captopril on α1-adrenoceptor mRNA and protein and phenylephrine-induced contraction was assessed in aorta of pre-hypertensive spontaneously hypertensive rats. 2 Four-week-old SHR and WKY rats were treated with captopril [an angiotensin-converting enzyme (ACE) inhibitor] 3 mg kg−1 day−1 for 1 week. 3 pA2 values for BMY 7378, an α1D-adrenoceptor antagonist, were 8.63–9.20 among the different groups. Schild slopes were close to unity suggesting that contraction was produced primarily by α1D-adrenoceptor stimulation and was not changed with therapy. 4α1D-Adrenoceptor mRNA and protein values were higher in pre-hypertensive SHR than in WKY, whereas α1A-adrenoceptor mRNA was higher in WKY and α1B-adrenoceptors were similar in both strains, and protein was not significantly different for α1A- and α1B-subtypes. 5 Captopril decreased maximal contraction in SHR, without having effect in WKY rats, while α1D-adrenoceptor mRNA was decreased in both rat strains but α1D-adrenoceptor protein was significantly decreased only in SHR, and increased α1A-mRNA in SHR, no effect of captopril treatment was observed on α1B-adrenoceptor mRNA and protein nor on α1A-adrenoceptor protein. 6 These data suggest that ACE inhibition by captopril influences both expression and function of α1D-adrenoceptors in aorta of pre-hypertensive rats, probably avoiding α1D-subtype expression by blockade of angiotensin II synthesis.