Na(+)-K(+)-ATPase inhibition sensitizes renal mechanoreceptors activated by increases in renal pelvic pressure.

Abstract

In anesthetized rats, the activation threshold of renal pelvic mechanoreceptors was determined by graded increases in renal pelvic pressure. Ipsilateral afferent renal nerve activity increased 9 +/- 4 (NS), 34 +/- 12, 47 +/- 8, 58 +/- 13, 68 +/- 14, and 91 +/- 17% (all P < 0.01) by the increase in renal pelvic pressure from 2.5 to 15 mmHg in 2.5-mmHg steps. Contralateral diuresis and natriuresis were elicited by renal pelvic pressures > 2.5 mmHg. Renal pelvic perfusion with 1.4 mM ouabain, an inhibitor of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase), increased basal afferent renal nerve activity transiently, lowered the activation threshold of renal mechanoreceptors to < 2.5 mmHg, and enhanced the afferent renal nerve activity, responses to increasing renal pelvic pressures by 8 and 30 mmHg. The afferent renal nerve activity response to increased renal pelvic pressure was also enhanced by renal pelvic perfusion with 900 mM NaCl but was unaltered by NaCl concentrations ranging from 10 to 600 mM. These findings show that renal pelvic mechanoreceptors are activated by increases in renal pelvic pressure within the physiological range. Although renal Na(+)-K(+)-ATPase contributes to the maintenance of the resting membrane potential of renal pelvic mechanoreceptors, the renal pelvic mechanoreceptor discharge is not influenced by physiological renal pelvic Na+ concentrations.