Impaired renal sensory responses after @entity8 in the XXXX .

@entity8 @entity10133 @entity8123 @entity63 @entity16325 @entity432 @entity35
Renal sensory responses and reflex function were examined in @entity35 24 h after 45 min of @entity63 caused by unilateral @entity432 ( @entity432 ). The integrity of renal pelvic mechanoreceptor (MRu)-mediated renorenal reflex was examined. An @entity8 (ARNA) and a reflex decrease in efferent @entity8 (ERNA) and contralateral diuresis and natriuresis produced by increasing the intrapelvic pressure were seen in sham-operated (Sham) @entity35 , but it was largely attenuated in @entity432 @entity35 . Using single-fiber recordings of the renal MRu discharge, graded increases in intrapelvic pressure or renal pelvic administration of substance @entity10133 ) resulted in pressure- or concentration-dependent increases in ARNA in the control kidney of Sham @entity35 , whereas attenuated responses were seen in the postischemic kidney of @entity432 @entity35 . The unresponsiveness of renal MRus in @entity432 @entity35 was accompanied by an insufficient release of SP. However, the baseline SP release is higher in @entity432 kidneys due to a reduced @entity8123 ( @entity8123 ) activity in the @entity8 . No changes in @entity16325 mRNA levels were demonstrated; however, the expression of NK-1 receptors in the plasma membrane of @entity432 pelvis were decreased, possibly resulting from the internalization of the receptors associated with beta-arrestin trafficking. Renal excretory responses after saline loading were significantly lower in the postischemic kidney of @entity432 @entity35 than in Sham @entity35 . Responses of ARNA and ERNA were also lower. It is concluded that the defective activation of renal sensory mechanoreceptors in the postischemic kidney results from an inadequate release of SP after mechanostimulation and the reduced functional NK-1 receptors.
