The effect of ureteral distension on peristalsis

Abstract

Isolated sheep and human ureteral preparations (from patients with bilharzia) were subjected in-vitro to graded elongation and the effect on tension and spontaneous peristaltic frequency was assessed. Sheep specimens were obtained from three locations: the intra- and extrarenal portion of the pelvis and distal ureter. Elongation (stretch) induced an increase in spontaneous frequency only in pelvic ureteric specimens, but not in the distal ureter. Basal tension increased exponentially with stretch and most markedly in the distal sheep ureter and also in human preparations. Active tension (amplitude of phasic contractions) increased with stretch in specimens from all locations and reached a maximum at 110-115% elongation. These data suggest that acute distension of the ureter increases frequency of peristaltic waves only in the intrarenal parts of the ureter. Acute obstruction in renal colic can induce hypermotility in terms of increased frequency and force of contraction.

Scintigraphic evidence of abnormal ureteric peristalsis following urological surgery

“…Surgical division and re-anastomosis of the ureter is accompanied by disruption of both the neural innervation and the ureteric smooth muscle. In this study surgery did not lead to the loss of ureteric peristalsis, which is consistent with experimental studies [3,4] and further supports the view that the autonomic innervation is not necessary for the conduction of peristalsis. However, we have shown that ureteric division and re-anastomosis does lead to a significant increase in retrograde conduction of peristalsis waves.…”

“…However, we have shown that ureteric division and re-anastomosis does lead to a significant increase in retrograde conduction of peristalsis waves. This is likely to be the consequence of surgical disruption of ureteric smooth muscle continuity and further supports an important role for myogenic conduction in ureteric peristalsis in man [2,3]. An alternative, if speculative, explanation is that the increased incidence of retrograde peristalsis is the consequence of loss of neural regulatory activity [a].…”

Protein Kinase 2β Is Expressed in Neural Crest-Derived Urinary Pacemaker Cells and Required for Pyeloureteric Contraction

“…HCN3+ and cKIT+ populations of utPMCs function sequentially to initiate and propagate pyeloureteric contractions. 2,3,5 Although the presence and spatial organization of utPMCs has been shown to be perturbed in congenital urinary tract malformations and particularly in hydronephrosis, 18,[23][24][25][26][27][28][29][30][31][32][33][34] little is known regarding the direct contribution of utPMCs to the pathobiology of these disorders. Lack of knowledge regarding the origin and development of utPMCs limits the ability to investigate these issues.…”

“…Whereas the expression of HCN3 has not been analyzed, cKIT expression is altered in ureteric tissue isolated from humans and experimental animals with congenital kidney diseases, including vesicoureteral reflux, ureteropelvic junction (UPJ) obstruction, primary obstructive megaureter, and nonobstructive hydronephrosis. [23][24][25][26][27][28][29][30][31][32][33][34] Analysis of proximal ureter tissue sections from children with UPJ obstruction undergoing pyeloplasty demonstrated decreased cKIT expression, 24,29,31 although primary obstructive megaureter tissues also exhibit significantly fewer cKIT+ cells compared with control samples. 30,33 The critical contribution of HCN3+ and cKIT+ utPMCs to urinary tract health and perturbation of these cells in congenital kidney diseases provides an impetus to elucidate mechanisms that control the specification and differentiation of these cells.…”

A Gender Comparison of Postobstructive Injury in the Rat Kidney

“…Ureteric hypercontractility occurs early after obstruction [1,2] and is followed by the progressive pooling of hypotonic urine [3] . Both of these mechanical stress stimuli are linked to the induction of apoptosis and inflammation and may give rise to reductions in renal perfusion and the establishment of tubulointerstitial fibrosis [4,5] .…”