Bradykinin and excitatory reno‐renal reflexes

The inflammatory mediator, bradykinin, when given into the renal artery elicits renal nerve dependent increases in renal vascular resistance. This study examined how renal interstitial bradykinin infusion regulated contralateral renal sympathetic nerve activity (RSNA) and the contribution of TRP channels in the response. Groups of chloralose/urethane anaesthetised male Wistar rats (n=6) were prepared for renal interstitial infusion at 1ml/h of bradykinin, 3×10 −9 g/L, 6×10 −9 g/L and 1.2×10 −8 g/L, into the ipsilateral kidney and measurement of RSNA to the contralateral kidney. Data, means±SEM were subject to two‐way ANOVA and significance taken at P<0.05. Bradykinin infusion had no effect on blood pressure, at 103±3mmHg, but increased RSNA from a basal value, 2.2±0.3mV/s, to 2.7±0.5, 3.1±0.6 and 4.0±0.6mV/s at the highest dose. The RSNA responses to bradykinin were abolished by denervation of the ipsilateral kidney and by co‐infusion of the TRP channel blocker, capsazepine, 5 μg/ml, with the bradykinin. These data demonstrate that bradykinin, which is associated with renal injury and failure, can activate sensory nerves within the kidney to elicit a renal sympatho‐excitation.