NA-K+-ATPASE INHIBITION SENSITIZES RENAL MECHANORECEPTORS ACTIVATED BY INCREASES IN RENAL PELVIC PRESSURE()

In anesthetized rats, the activation threshold of renal pelvic mechano receptors 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-mm Hg steps. Contralateral diuresis and natriuresis were elicited by rena l pelvic pressures > 2.5 mmHg. Renal pelvic perfusion with 1.4 mM ouab ain, an inhibitor of Na+-K+-adenosinetriphosphatase (Na+-K+-ATPase), i ncreased basal afferent renal nerve activity transiently, lowered the activation threshold of renal mechanoreceptors to <2.5 mmHg, and enhan ced the afferent renal nerve activity responses to increasing renal pe lvic pressures by 8 and 30 mmHg. The afferent renal nerve activity res ponse to increased renal pelvic pressure was also enhanced by renal pe lvic perfusion with 900 mM NaCl but was unaltered by NaCl concentratio ns ranging from 10 to 600 mM. These findings show that renal pelvic me chanoreceptors are activated by increases in renal pelvic pressure wit hin the physiological range. Although renal Na+-K+-ATPase contributes to the maintenance of the resting membrane potential of renal pelvic m echanoreceptors, the renal pelvic mechanoreceptor discharge is not inf luenced by physiological renal pelvic Na+ concentrations.