Intrarenal bradykinin elicits reno‐renal reflex sympatho‐excitation and renal nerve‐dependent fluid retention

Aims The renal sensory nerves are importantly involved in the sympathetic regulation of cardiovascular and renal function. Two reno‐renal reflexes are recognized, one in which activation of renal sensory nerves elicits a renal sympatho‐inhibition, and one which causes a renal sympatho‐excitation and about which little is known. This study investigated the role of bradykinin ( BK ) in engaging an excitatory reno‐renal reflex. Methods Rats were anaesthetized (chloralose/urethane) and prepared for the measurement of renal function or renal sympathetic nerve activity ( RSNA ). BK was infused into the cortico‐medullary border of the ipsilateral kidney and the impact on contralateral renal function and RSNA evaluated. Results Intrarenal infusion of BK at 3 × 10 −9 and 6 × 10 −9  g L −1 had no effect on mean arterial pressure, at 104 ± 5 mmHg or glomerular filtration rate in either the ipsilateral or contralateral kidneys, at 4.31 ± 0.45 mL min −1  kg −1 . At the highest dose of BK , fractional sodium excretion ( FEN a) was 1.47% in the ipsilateral kidney and was significantly lower, at 0.64% ( P  < 0.05) in the contralateral kidney but this difference did not occur following ipsilateral renal denervation. Ipsilateral intrarenal infusion of BK at 3 × 10 −9 , 6 × 10 −9 and 1.2 × 10 −8  g L −1 elicited dose‐related increases ( P  < 0.05) in contralateral RSNA , reaching some 78% at the highest dose, but these responses were prevented by ipsilateral renal denervation. Conclusions Intrarenal infusion of BK produced an excitatory reno‐renal reflex which was expressed as a renal nerve‐dependent antinatriuresis in the contralateral kidney. The findings suggest that inflammatory mediators such as BK may be important in initiating a sympatho‐excitation associated with renal and cardiovascular diseases.