TRPV1-mediated diuresis and natriuresis induced by hypertonic saline perfusion of the renal pelvis.

BACKGROUND

The transient receptor potential vanilloid type 1 (TRPV1) channel is known to be activated by multiple stimuli, albeit its role in mediating renal function is largely unknown. This study was designed to test the hypothesis that TRPV1 mediates diuresis and natriuresis induced by hypertonic saline perfusion into the pelvis.

METHODS

NaCl or KCl was perfused into the left renal pelvis of rats at a rate without changing renal pelvic pressure. Afferent renal nerve activity (ARNA), urine flow rate (V) and urinary sodium excretion (UNaV) in the presence or absence of selective antagonists of TRPV1, capsazepine (CAPZ), or neurokinin-1 (NK1) receptors, RP67580, were examined.

RESULTS

Unilateral renal pelvis perfusion of NaCl at 600 mM, but not 150 or 300 mM, increased ipsilateral ARNA and contralateral V and UNaV, which were blocked by ipsilateral administration of CAPZ or RP67580. In contrast, KCl perfused at 150 or 300 mM, but not 600 mM, increased ipsilateral ARNA and contralateral V and UNaV, which were insensitive to CAPZ.

CONCLUSION

Unilateral hypertonic saline perfusion causes contralateral diuresis and natriuresis via TRPV1 or NK1 activation, indicating that these receptors may play a critical role in sensing microenvironmental changes in the renal pelvis to modulate renal function in health and disease.