Key result
Captopril attenuates evoked 3H efflux and contraction in guinea-pig pulmonary arteries independent of intrinsic angiotensin.
In guinea-pig pulmonary arteries, captopril attenuates presynaptic adrenergic transmission through a mechanism likely independent of ACE inhibition or prostaglandins.
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Captopril's non-ACE presynaptic effects in guinea-pig arteries warrant no clinical changes; leaves open non-angiotensin mechanisms for future human studies.
Yasuda et al. (1987) studied this question. Captopril was evaluated on 3H efflux and contraction evoked by transmural field stimulation. Captopril attenuated evoked 3H efflux and contraction in guinea-pig pulmonary arteries, but this presynaptic adrenergic transmission failure appears independent of an intrinsic angiotensin system.
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