Bezold–Jarisch reflex

von Bezold and Hirt described a reaction comprising a triad of bradycardia, hypotension, and apnea (hypopnea) resulting from an intravenous injection of an alkaloidal extract of Veratrum viride or Viscum album in 1867.

[4] This observation was comparatively neglected until Jarisch and Henze re-examined it in 1937; they identified the reaction as a chemoreflex acting via the vagus nerve that was relayed in the nucleus tractus solitarii (NTS), and termed it the Bezold reflex.

The myelinated afferents originating in the atria are attached to discrete receptor endings, whereas most of the unmyelinated fibers are located in the ventricles and the walls of the coronary vessels.

[8][7][9] The sites of the chemoreflex and baroreflex input overlap and there is evidence that these reflexes modify each other, probably through the actions of excitatory and inhibitory neurotransmitters, such as serotonin and Gamma-Aminobutyric acid (GABA).

[7][9] Although the reflex was originally described in response to Veratrum alkaloids, it can be stimulated by many biologically active chemicals, including nicotine, capsaicin, bradykinin, atrial natriuretic peptide, prostanoids, nitrovasodilators, angiotensin II type 1 receptor (AT1) antagonists and serotonin agonists.