Angiotensin II potentiates neurally mediated contraction of rabbit airway smooth muscle.

The effect of angiotensin II (AT II) on cholinergic neurotransmission in rabbit tracheal segments was studied under isometric conditions in vitro. AT II concentration-dependently potentiated the contractile response to electrical field stimulation (EFS), and caused a leftward shift of the frequency-response curves for EFS, so that the stimulus frequency required to produce a half-maximal effect (ES50), decreased from 7.0 +/- 0.1 to 3.0 +/- 0.1 Hz (P less than 0.01). In contrast, the contractile response to acetylcholine was not affected. Non-peptide AT II receptor antagonist CV-2961 attenuated the effect of AT II on the EFS-induced contraction. Pretreatment of tissues with thiorphan or phosphoramidon did not alter the action of AT II. Thus, AT II may prejunctionally potentiate the neurally-mediated contraction of airway smooth muscle through activation of AT II receptors on the cholinergic nerve terminals, and this effect may not be modulated by endogenous neutral endopeptidase.