Key points are not available for this paper at this time.
A persistent question with regard to the effects of catecholamines on baroreceptor activity has been whether the adrenergic action is indirectly mediated through an alteration in vessel wall tone or whether it is a direct action on the excitability of baroreceptor nerve endings. The effects of norepinephrine on the pressure-impulse frequency relationship of rat single aortic baroreceptor fibers were studied in vitro. Perfusion of the aortic arch with norepinephrine produced an excitatory response which consisted of: a drug-evoked stimulation of previously quiescent fibers at 0 mm Hg, and a sensitization of the response to pressure. The norepinephrine-induced facilitation was blocked by prazosin but not by yohimbine. Phenylephrine mimicked the effects of norepinephrine, whereas clonidine had no excitatory effects on baroreceptor activity. Baroreceptor activity was unaffected by beta-adrenergic agonists or antagonists. Norepinephrine had no effect on the pressure-volume relationship of the aortic arch, but produced a contraction of helical aortic strips. However, there was no correlation between the concentration-response relationship of norepinephrine on aortic smooth muscle and its excitatory action on baroreceptors. 5-Hydroxytryptamine and angiotensin II produced a contraction of helical strips, but had no effect on baroreceptor activity. Sodium nitrate reduced the norepinephrine-induced contractile response by 75%, but did not antagonize the baroreceptor facilitation. It is proposed that the excitatory action of norepinephrine is independent of smooth muscle activity, and is mediated by activation of alpha 1-adrenergic receptors located on the aortic baroreceptor nerve endings.
Goldman et al. (Sun,) studied this question.