Authors:Fares Osman, I. Romics, P. Nyírády, E. Monos and GyL. Nádasy
The pyeloureteral function is to transport urine from the kidneys into the ureter toward the urinary bladder for storage until micturition. A set of mechanisms collaborates to achieve this purpose: the basic process regulating ureteral peristalsis is myogenic, initiated by active pacemaker cells located in the renal pelvis. Great emphasis has been given to hydrodynamic factors, such as urine flow rate in determining the size and pattern of urine boluses which, in turn, affect the mechanical aspects of peristaltic rhythm, rate, amplitude, and baseline pressure. Neurogenic contribution is thought to be limited to play a modulatory role in ureteral peristalsis. The myogenic theory of ureteral peristalsis can be traced back to Engelmann (1) who was able to localize the peristaltic pressure wave’s origin in the renal pelvis and suggested that the ureteral contraction impulse passes from one ureteral cell to another, the whole ureter working as a functional syncitium. Recent studies of ureteral biomechanics, smooth muscle cell electrophysiology, membrane ionic currents, cytoskeletal components and pharmacophysiology much improved our understanding of the mechanism of how the urine bolus is propelled, how this process is disturbed in pathological states, and what could be done to improve it.
Authors:Levente Sára, GyL. Nádasy, P. Antal, M. Szekeres, A. Monori-Kiss, E. Horváth, A. Tőkés, G. Masszi, E. Monos and Szabolcs Várbíró
To clarify the effects of dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS) on arteriolar biomechanics in a rat model and the possible modulatory role of vitamin D3.Methods and Results The PCOS model was induced in female Wistar rats by ten-weeks DHT treatment. Arteriolar biomechanics was tested in arterioles by pressure arteriography in control as well as DHT- and DHT with vitamin D3-treated animals in contracted and passive conditions. Increased wall stress and distensibility as well as increased vascular lumen were detected after DHT treatment. Concomitant vitamin D3 treatment lowered the mechanical load of the arterioles and restored the vascular diameter.Conclusion The hyperandrogenic state resulted in more rigid, less flexible arteriolar walls with increased vascular lumen compared with controls. DHT treatment caused eutrophic remodelling of gracilis arteriole. These prehypertensive alterations caused by chronic DHT treatment were mostly reversed by concomitant vitamin D3 administration.