Arginine vasopressin (AVP) reportedly enhances, whereas angiotensin II (ANG II) attenuates, baroreflex control of the circulation. Here we examine whether these responses can be attributed, in part, to local actions on myelinated baroreceptor (BR) afferents, either directly or via changes in vascular tone. An in vitro rabbit aortic arch/aortic nerve preparation was used to study regularly discharging presumably myelinated BRs under controlled static and pulsatile pressures. At constant suprathreshold pressures, AVP (10(-13) M to 10(-6) M) had no effect on arch diameter or BR frequency, whereas equimolar concentrations of ANG II evoked dose-dependent vasoconstriction and associated BR inhibition. Differences were not caused by limited diffusion to BR endings lying outside the media, since similar results were obtained with either luminal or adventitial applications. AVP also had no effect on diameter or discharge in arches preconstricted with norepinephrine, whereas acetylcholine (ACh) relaxed the arch and thereby increased BR activity. These results eliminate possible AVP-induced endothelium-dependent vasodilation or potentiation of adrenergic vasoconstriction that would not be evident in isolated arches lacking tone. Finally, AVP did not sensitize BRs to changes in pressure, since ramp-evoked pressure-discharge curves remained constant and pulsatile discharge in response to sine-wave pressure inputs was unaltered. ANG II, however, shifted pressure-discharge curves to higher pressures and, with pulsatile inputs at constant mean pressure, reduced peak and average discharge firing rates. In conclusion, AVP has no apparent peripheral effect on aortic myelinated BRs in rabbits that could contribute to amplification of the baroreflex when AVP levels are elevated. In contrast, ANG II can inhibit BR firing as a consequence of local vasoconstriction, which may contribute to attenuation of the reflex when ANG II levels are elevated.