title: Impaired renal sensory responses after unilateral ureteral obstruction in the rat.
abstract: Renal responses to the activation of renal sensory receptors were examined in rats after release of 24-h unilateral ureteral obstruction of the left kidney. The integrity of the renorenal reflex was examined in both 24-h unilateral ureteral obstruction-treated (UUO) and sham-operated (Sham) rats. Increased ipsilateral afferent renal nerve activity (ARNA) and reflexly decreased efferent renal nerve activity (ERNA) and increased contralateral diuresis and natriuresis produced by increasing the left intrapelvic pressure were observed in Sham rats but not in UUO rats. The lack of responsiveness of the renorenal reflex in UUO rats was associated with lower release of substance P (SP) and increased neutral endopeptidase (NEP) activity in the renal pelvis in the postobstructive kidney. Compared with Sham rats, urine and sodium excretion after acute saline loading was significantly reduced in the postobstructive kidney. The blunted excretory responses were accompanied by lower activation of ARNA and less reflex inhibition of ERNA. Renal sensory dysfunction in the postobstructive kidney was further examined by stimulation of renal mechanoreceptors and chemoreceptors. Graded increases in intrapelvic pressure or renal pelvic perfusion with hypertonic saline solution elicited, respectively, a pressure- or concentration-dependent increase in ARNA in the control kidney of Sham rats, this response being greatly attenuated in the postobstructive kidney. Western blots showed no quantitative difference in the expression of renal pelvic neurokinin 1 (NK-1) receptors between the two groups. It was concluded that renal sensory function is impaired in the postobstructive kidney of UUO rats and that this defective activation of renal sensory receptors results in an impaired renorenal reflex, which is associated with enhanced NEP activity and catabolism of SP released in the renal pelvis and is not related to the expression of NK-1 receptor protein.
authors.affiliation: *Department of hysiology, College of Medicine, National Taiwan University, Taipei, Taiwan; and Department of Urology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Ming-Chieh
authors.initials: MC
authors.lastname: Ma
authors.affiliation: *Department of hysiology, College of Medicine, National Taiwan University, Taipei, Taiwan; and Department of Urology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Ho-Shiang
authors.initials: HS
authors.lastname: Huang
authors.affiliation: *Department of hysiology, College of Medicine, National Taiwan University, Taipei, Taiwan; and Department of Urology, National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Chau-Fong
authors.initials: CF
authors.lastname: Chen
mesh_terms: D000344:Afferent Pathways / Q000187:drug effects / Q000503:physiopathology; D000818:Animals; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000503:physiopathology; D004525:Efferent Pathways / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D015151:Immunoblotting; D007668:Kidney / Q000294:innervation / Q000503:physiopathology*; D007682:Kidney Pelvis / Q000378:metabolism; D008465:Mechanoreceptors / Q000187:drug effects / Q000503:physiopathology; D009318:Natriuresis / Q000187:drug effects; D015260:Neprilysin / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D012018:Reflex; D012677:Sensation; D012965:Sodium Chloride / Q000494:pharmacology; D013373:Substance P / Q000378:metabolism; D014517:Ureteral Obstruction / Q000503:physiopathology*
chemical_list: D018040:Receptors, Neurokinin-1; D013373:Substance P; D012965:Sodium Chloride; D015260:Neprilysin