Perivascular nerves induce cardiorespiratory reflexes in response to algogens

In the present study we measured cardiovascular and respiratory reflexes evoked by administration of bradykinin and capsaicin into the hindlimb vasculature of anaesthetised rats, whilst simultaneously recording activity of sensory afferents on the adventitial surface of femoral arteries and veins. Bradykinin (0.9 nmol) and capsaicin (0.3 nmol) caused a rapid reflex fall in mean arterial pressure (delta mmHg: -37 +/- 8 and -28 +/- 3, respectively; P < 0.01) and an increase in respiratory minute volume (delta ml min(-1): 180.0 +/- 39.2 and 156.1 +/- 24.5, respectively; P < 0.01), associated with an increase in neural discharge in arterial afferents (from basal 0.4 +/- 0.3 to 8.5 +/- 2.9 impulses s(-1) following intra-arterial administration of bradykinin, P < 0.05, n = 7; from basal 0.2 +/- 0.1 to 7.5 +/- 3.7 impulses s(-1) with capsaicin, P < 0.01, n = 18). The antagonists FR173657 and capsazepine confirmed bradykinin B2 and vanilloid VR1 receptors mediated the responses to bradykinin and capsaicin, respectively. Topical administration of algogen to the vessel surface, and electrical stimulation of the adventitia also evoked cardiovascular and respiratory responses. These data support the hypothesis that stimulation of sensory nerve endings within the hindlimb vasculature contributes to systemic cardiorespiratory reflexes in the rat.