|
|
|
118 |
|
|
|
|
|
|
|
|
|
Practical Urology: EssEntial PrinciPlEs and PracticE |
|
Table 8.1. Various substances |
and their effect on ureteral |
Ramsey et al., however, demonstrated in vitro |
||
contraction |
|
that urine tends to drain around stents rather |
||
Substance |
Effect |
than through them, suggesting that luminal size |
||
acetylcholine |
contraction |
is less of a clinical concern.29 Clayman exam- |
||
ined both standard double pigtail as well as |
||||
|
|
|
||
a-agonists |
contraction |
specialty stents, and determined that only stan- |
||
b-agonists |
relaxation |
dard stent configurations flow based on luminal |
||
diameter.30 |
||||
|
|
|
||
neurokinin a and B |
contraction |
Ureteral stents have been shown to decrease |
||
PgF2a |
contraction |
ureteral peristalsis. As such, ureteral calculi are |
||
less likely to pass while in the stented ureter.31 |
||||
Pgd2 |
contraction |
Notably, Stoller et al. demonstrated an increased |
||
tXa2 |
contraction |
stone passage rate using spiral-ridged stents as |
||
compared to traditional double pigtail stents.31 |
||||
PgE2 |
21contraction in obstruction, |
|||
In general, ureteral stents are placed often to |
||||
|
|
relaxation in normal |
allow gradual passage of stones to avoid |
|
PgE1 |
relaxation |
Steinstrausse formation. |
||
|
||||
Physiologic Implications
of Ureteral Obstruction
Ureteral obstruction has profound effects on the ureter. Obstruction, whether from a stone or other source, results in stimulation of afferent sensory neurons reacting to stretch and distention of the ureter. Along with pain, the stretch causes an increase in the rate and amplitude of contractions. It has been shown in rats that partial ureteral obstruction causes a 500% increase in the amplitude of ureteral contractions in a rat model.24 Ureteral obstruction also affects renal function and blood flow. It has been shown in animal models that unilateral complete obstruction result in complete loss of function in the renal unit if the obstruction lasts more than 6 weeks.25
Ureteral stents provide drainage of the upper tracts in cases of obstruction. Studies of ureteral stents have broadened our understanding of the physiology of ureteral obstruction. In a porcine model of the stented ureter, normal peristalsis disappeared for days 1 and 2, then became irregular after day 5.26 In general, ureteral peristalsis is increased initially in response to stent placement but ultimately is largely reduced or completely eliminated.27
There have been multiple studies investigating flow patterns in the stented ureter. Mardis et al. observed that stents with larger luminal diameter and side holes provided better drainage.28
Ureteral Pharmacology
Ureteral pharmacology has been studied since 1970. The long accepted premise that ureteral spasm and increased contractility cause pain was demonstrated by Laird et al. in 1997.32 This leads to efforts to achieve targeted therapy to reduce ureteral spasm via the known physiologic pathways of ureteral contraction.
Opioids have traditionally been utilized to control the symptoms associated with ureteral obstruction. They work by activating mu receptors and thus blocking the afferent pain pathways caused by ureteral obstruction. Interestingly, however, some studies have revealed a spasmogenic effect of opioids on the ureter,33 so clearly their effect on pain relief is not related to ureteral relaxation.
Prostaglandins are generally potent contractants of smooth muscle. As such, agents such as nonsteroidal anti-inflammatories (NSAIDS) have been successful in inhibiting ureteral contractility in multiple studies.34 Both nonselective COX inhibitors and selective COX-2 inhibitors have been shown to decrease ureteral contraction.35 Because COX-2 expression is up regulated in inflammation and obstruction, inhibition of COX-2 is successful in relaxing the ureter in these circumstances. In addition, celecoxib as well as indomethacin have been shown to inhibit prostaglandin release in the ureter, even when
119
UrEtEral Physiology and Pharmacology
COX-2 was upregulated.20 Despite the clear |
doxazosin and found that they increased stone |
effect on ureteral contractility, the clinical use of |
passage rate from 52% to 79%, 78%, and 75%, |
NSAIDS may be limited due to their effect on |
respectively.42 |
renal function. Because prostacyclin-driven |
Numerous randomized studies have exam- |
contralateral renal vasodilation in cases of |
ined tamsulosin compared to either nifedipine |
obstruction is dependent on COX-2, blocking |
or placebo for expulsive therapy. In these stud- |
this pathway has the potential to lead to a high |
ies the stone passage rate was 97–100% com- |
rate of renal insufficiency.14 |
pared to 64–70% in the placebo groups.43,44 |
Phosphodiesterase (PDE) inhibitors produce |
Tamsulosin offered a 20% increase in passage |
significant effects on ureteral contractility.36 |
rate when compared to nifedipine.45 In gen- |
PDE enzymes degrade cAMP and cGMP, and |
eral, studies thus far favor the use of alpha |
blocking this process leads to accumulation of |
blockers over calcium channel blockers due to |
these nucleotides and subsequent smooth mus- |
efficacy and a low side effect profile. In 2006, |
cle relaxation by activation of protein kinase A |
Hollingsworth and colleagues published a |
and phosphorylation of myosin light chain |
meta-analysis of nine randomized controlled |
kinase. There are seven isoforms of PDE, but |
trials investigating the use calcium channel |
inhibition of PDE-IV has been shown to have |
blockers and alpha blockers. Compared with |
the greatest effect on ureteral relaxation.37 |
the control group, patients treated with nife- |
Calcium channel blockers have been pro- |
dipene or tamsulosin had an overall 65% |
posed as a method for inhibiting ureteral con- |
greater likelihood of stone passage.46 A subse- |
traction and thus reducing pain in situations of |
quent meta-analysis from the combined AUA/ |
obstruction. Nifedipine and verapamil have |
EUA ureteral stone guidelines demonstrated |
been studied and interestingly found to inhibit |
an increase in passage rate for nifedipine of |
fast phasic contractions while preserving slow |
9% which was not statistically significant. |
phasic contractions,38 thus preventing spasm |
Meta-analysis of tamsulosin versus control |
while maintaining normal peristalsis. For this |
demonstrated an absolute increase in passage |
reason, nifedipine has been investigated as a |
rate of 29% which was significant.47 |
stone expulsive agent. In one study, nifedipine |
Most alpha blocker studies have included the |
was shown to increase stone passage rate from |
use of steroids in their study groups. A random- |
65% to 87%.39 In another series, 96 patients with |
ized trial of 60 patients to either alpha blockers |
distal ureteral stones received either deflazacort |
and steroids or steroids alone found no differ- |
and nifedipine or conservative management. |
ence in overall passage rate, but a more rapid |
Stone expulsion rate in the nifedipine group was |
rate of passage in the steroid group (72 vs |
79% compared to 35% in the conservatively |
120 h).48 In general, steroids provide some ben- |
managed group. Mean time to stone passage was |
efit as expulsive therapy when combined with |
7 days in the nifedipine groups versus 20 days in |
other agents, but not alone.46 Moreover, there is |
the conservative group.40 Despite the clear |
even evidence to suggest that alpha blockers |
increase in stone passage rate, there is no evi- |
contribute to analgesia in cases of obstruction. |
dence that calcium channel blockers contribute |
Tamsulosin has been shown to decrease discom- |
to pain control from obstruction. One study |
fort associated with shockwave lithotripsy as |
evaluated nifedipine versus placebo in 30 |
well as steinstrasse which develops following |
patients with renal colic and found no signifi- |
shockwave lithotripsy.49,50 |
cant difference in pain control.41 |
An important finding is that alpha antago- |
There is a significant body of literature to sup- |
nists cause complete relaxation of the ureter |
port alpha antagonists as expulsive agents for |
only in the presence of epinephrine (the endog- |
stones.Alpha antagonists can be broadly grouped |
enous ligand of beta and alpha receptors).51 This |
into either selective or nonselective, depending |
phenomenon suggests a role of beta adrenergic |
on their affinity for alpha 1A and 1D receptors, |
receptors in ureteral relaxation, as unopposed |
which are abundant in the ureter. Both nonselec- |
beta stimulation seems to have an effect on ure- |
tive and selective alpha antagonists have been |
teral relaxation. For this reason, future studies |
shown to effectively reduce ureteral spasm. |
of expulsive therapy will likely include beta |
Yilmaz et al. studied tamsulosin, terazosin, and |
agonists. |
|
|
120 |
|
|
|
|
|
|
|
Practical Urology: EssEntial PrinciPlEs and PracticE |
|
Neurokinin receptor antagonists have been |
Special Situations |
||
|
|||
studied in vitro as alternative agents to modu- |
in Ureteral Physiology |
||
late ureteral contractility. The three neuroki- |
|||
nin receptors, NK1, NK2, and NK-3 have |
|
||
affinity for substance P, neurokinin A and |
Infection of the upper tract has been shown |
||
neurokinin B, respectively.52 Blockage of these |
in vitro and in vivo to impair ureteral contrac- |
||
receptors prevents phospholipase C synthesis |
tion. As early as 1913, Primbs demonstrated that |
||
and ultimately calcium influx into the smooth |
toxins released by E. coli and staphylococcus |
||
muscle cell. The result is ureteral relaxation.52 |
had the ability to inhibit contractions in the |
||
NK-2 is the predominant receptor in the |
guinea pig ureter.57 In humans, decreased peri- |
||
human ureter, and its inhibition in vitro pre- |
stalsis and even absence of peristalsis has been |
||
vents ureteral contractility.52 NK-2 blockade |
documented in the ureter in cases of infection, |
||
has yet to be studied clinically, but if safe may |
and can be a radiographic disease hallmark.58 |
||
decrease obstruction-related pain and |
Not surprisingly, ureteral contractility and |
||
increase stone passage rates. |
ureter response to various stimuli changes with |
||
Nitric oxide (NO) is a major inhibitory neu- |
age. In vitro studies have observed that an |
||
rotransmitter in the ureter. Based on axons that |
intraluminal pressure load will cause more |
||
stain positive for nitric oxide synthase in the |
deformation in a neonatal rabbit ureter than in |
||
human ureter, it has been suggested that nitric |
an adult.59 In addition, there seems to be a |
||
oxide may play a role in ureteral relaxation.53 |
decrease in the response of the ureter to Beta |
||
In vitro, it has been shown that NO inhibits |
adrenergic agents with age, an event likely medi- |
||
ureteral contractility in rats.54 Interestingly, |
ated by decreased cAMP levels.60 |
||
NO seems to play a specific role at the ure- |
Pregnancy has been known to cause varying |
||
terovesical junction, where it has been postu- |
degrees of hydroureteronephrosis, although the |
||
lated to regulate the valve-like effect in this |
mechanism of this phenomenon has been debated |
||
area.55 |
over time. Likely, a combination of obstruction |
||
Other pharmacological agents being studied |
and hormonal changes are responsible. Evidence |
||
in vitro include histamine antagonists, 5-HT |
for obstructive hydronephrosis includes the fact |
||
receptor antagonists, neuropeptides, Vasoactive |
that pregnant women demonstrate elevated rest- |
||
intestinal polypeptide, Calcitonin Gene-related |
ing pressures in the ureter above the pelvic brim, |
||
Peptide, Neuropeptide Y, and agents which effect |
which can be reversed with positional changes. In |
||
the Rho Kinase pathway. Each of these agents |
addition, hydronephrosis of pregnancy does not |
||
has the common endpoint of a decrease in ure- |
occur in quadriplegic patients, whose uterus |
||
teral contractility. Multiple experimental mod- |
hangs away from the ureters.61 Evidence for hor- |
||
els have been created to measure ureteral |
monaleffectsontheureterisconflicting.Although |
||
contractility and thus aid our understanding of |
some studies have demonstrated increased ure- |
||
these myriad agents56 (Table 8.2). |
teral dilatation due to progesterone, others have |
||
|
|
failed to show any correlation.61 In general, |
|
|
|
obstruction appears to be the primary factor in |
|
Table 8.2. Experimental agents for medical expulsive therapy |
hydronephrosis of pregnancy, although hor- |
||
mones may play a secondary role.61 |
|||
|
|
||
Beta agonists
neurokinin receptor antagonists nitric oxide
histamine antagonists 5-ht receptor antagonists neuropeptides
Vasoactive intestinal peptide calcitonin gene-related peptide
Conclusion
Ureteral physiology involves a complex interplay between various tissues, cells, receptors, and proteins. Clinical modulation of ureteral contraction has great promise for managing ureteral colic as well as expanding our understanding of medical expulsive therapy. To date, the most promising agents remain NSAIDS, alpha blockers, PDE-IV inhibitors, and NK
121
UrEtEral Physiology and Pharmacology
antagonists. More work on the subject is neces- |
17. |
Martin TV, Wheeler MA, Weiss RM. Neurokinin induced |
||
sary to determine the optimal agent or combi- |
|
inositol phosphate production in guinea pig bladder. J |
||
nation of agents to treat the human ureter. |
|
Urol. 1997;157:1098. |
||
18. |
Jerde TJ, Saban R, Bjorling DE, et al. Distribution of neu- |
|||
|
|
|||
|
|
|
ropeptides, histamine content, and inflammatory cells in |
|
References |
|
the ureter. Urology. 2000;56:173. |
||
19. |
Nakada SY, Jerde TJ, Bjorling DE, et al. In vitro contrac- |
|||
|
|
|
tile effects of neurokinin receptor blockade in the human |
|
1. |
Weiss RM. Physiology and pharmacology of the renal |
|
ureter. J Urol. 2001;166:1534. |
|
|
pelvis and ureter. In: Walsh PC, Retik AB, Vaughan ED, |
20. |
Jerde TJ, Calamon-Dixon JL, Bjorling DE, et al. Celecoxib |
|
|
Wein A, eds. Campbell’s Urology. Philadelphia, PA: WB |
|
inhibits ureteral contractility and prostanoid release. |
|
|
Saunders; 1998:839-869. |
|
Urology. 2005;65:185. |
|
2. |
Birder L. Role of the urothelium in bladder function. |
21. |
Ankem MK, Jerde TJ, Wilkinson ER, Nakada SY. Third |
|
|
Scand Urol J. 2004;215:48-53. |
|
prize: prostaglandin E(2)-3 receptor is involved in ure- |
|
3. |
Morita T, Ando M, Kihara K, Oshima H. Function and |
|
teral contractility in obstruction. J Endourol. |
|
|
distribution of autonomic receptors in canine ureteral |
|
2005;19:1088-1091. |
|
|
smooth muscle. Urol Int. 1995;55:123-127. |
22. |
Solari V, Piotrowska AP, Puri P. Altered expression of |
|
4. |
Kabalin JN. Surgical anatomy of the retroperitoneum, |
|
interstitial cells of Cajal in congenital ureteropelvic |
|
|
kidneys,and ureters.In:Walsh PC,Retik AB,Vaughan ED, |
|
junction obstruction. J Urol. 2003;170:2420. |
|
|
Wein A, eds. Campbell’s Urology. Philadelphia, PA: WB |
23. |
Murakumo M,Nonomura K,Yamashita T,et al.Structural |
|
|
Saunders; 1998:49. |
|
changes of collagen components and diminution of |
|
5. |
Yoshimura N, Chancellor M. Physiology and pharmacol- |
|
nerves in congenital ureteropelvic junction obstruction. |
|
|
ogy of the bladder and urethra. In: Walsh PC, Retik AB, |
|
J Urol. 1997;157:1963. |
|
|
Vaughan ED, Wein A, eds. Campbell’s Urology. |
24. |
Laird JM, Roza C, Cervero F. Effects of artificial calculo- |
|
|
Philadelphia, PA: WB Saunders; 2008:1923-1926. |
|
sis on rat ureter motility: peripheral contribution to the |
|
6. |
Andersson R, Nilsson K. Cyclic AMP and calcium in |
|
pain of ureteric colic. Am J Physiol. 1997; 272(R):1409. |
|
|
relaxation in intestinal smooth muscle. Nat New Biol. |
25. |
Vaughan ED Jr,Shenasky JHI,Gillenwater JY.Mechanism |
|
|
1972;238:119. |
|
of acute hemodynamic response to ureteral occlusion. |
|
7. |
Longrigg N. Minor calyces as primary pacemaker sites |
|
Invest Urol. 1971;9:109. |
|
|
for ureteral activity in man. Lancet. 1975;1:253. |
26. |
Roshani H, Dabhoiwala NF, Dijkhus T, et al. |
|
8. |
Davidson ME, Lang RJ. Effects of selective inhibitors of |
|
Pharmacological modulation of ureteral peristalsis in a |
|
|
cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX- |
|
chronically instrumented conscious pig model. I: Effect |
|
|
2) on the spontaneous myogenic contractions in the |
|
of cholinergic stimulation and inhibition. J Urol. |
|
|
upper urinary tract of the guinea-pig and rat. Br J |
|
2003;170:264. |
|
|
Pharmacol. 2000;129(4):661-670. |
27. |
Venkatesh R, Landman J, Minor SD, et al. Impact of a |
|
9. |
O’Conor VJ Jr, Dawson-Edwards P. Role of the ureter in |
|
double-pigtail stent on ureteral peristalsis in the porcine |
|
|
renal transplantation I: studies of denervated ureter |
|
model: initial studies using a novel implantable mag- |
|
|
with particular reference to ureterouerteral anastamo- |
|
netic sensor. J Endourol. 2005;19:170. |
|
|
sis. J Urol. 1959;82:566. |
28. |
Mardis HK, Kroeger RM, Hepperlen TW, Mazer MJ, |
|
10. |
Lang RJ, Exintaris B, Teele ME, et al. Electrical basis of |
|
Kammandel H. Polyethelene double-pigtail ureteral |
|
|
peristalsis in the mammalian upper urinary tract. Clin |
|
stents. Urol Clin N Am. 1982;9:95-101. |
|
|
Exp Pharmacol Physiol. 1998;25:310. |
29. |
Payne SR, Ramsay JW. The effects of double J stent of |
|
11. |
David SG, Cebrian C,Vaughan ED Jr, et al. c-kit and ure- |
|
renal pelvic dynamics in the pig. J Urol. 1988;140: |
|
|
teral peristalsis. J Urol. 2005;173:292. |
|
637-641. |
|
12. |
Lang RJ, Davidson ME, Exintaris B. Pyeloureteral motil- |
30. |
Olweny EO, Portis AJ,Afane JS, et al. Flow characteristics |
|
|
ity and ureteral peristalsis: essential role of sensory |
|
of 3 unique ureteral stents: investigation of a Poiseuille |
|
|
nerves and endogenous prostaglandins. Exp Physiol. |
|
flow pattern. J Urol. 2000;164:2099-2103. |
|
|
2002;87:129. |
31. |
Stoller ML, Schwartz BF, Frigstad JR, et al. An in vitro |
|
13. |
Tomiyama Y, Wanajo I, Tamazaki Y, et al. Effects of cho- |
|
assessment of the flow characteristics of spiral-ridged |
|
|
linergic drugs on ureteral function in anesthetized dogs. |
|
and smooth-walled JJ ureteric stents. BJU Int. |
|
|
J Urol. 2004;172:1520. |
|
2000;85:628-631. |
|
14. Hernandez M, Prieto D, Simonsen U, et al. Noradrenaline |
32. |
Laird JM, Roza C, Cervero F. Effects of artificial calculo- |
||
|
modulates smooth muscle activity of the isolated intra- |
|
sis on rat ureter motility: peripheral contribution to the |
|
|
vesical ureter of the pig through different types of adreno- |
|
pain of ureteric colic. Am J Physiol. 1997;272: |
|
|
ceptors. Br J Pharmacol. 1992;107:924. |
|
R1409-R1414. |
|
15. |
Peters HJ, Eckstein W. Possible pharmacological means |
33. |
Kaplan N, Elkin M, Sharkey J. Ureteral peristalsia and |
|
|
of treating renal colic. Urol Res. 1975;3:55. |
|
the autonomic nervous system. Investig Urol. 1968;5:468- |
|
16. |
Wanajo I, Tomiyama Y, Yamazaki Y, et al. Pharmaco- |
|
482. |
|
|
logical characterization of beta-adrenoceptor subtypes |
34. |
Cole RS, Fry CH, Shuttleworth KE. The action of prosta- |
|
|
mediating relaxation in porcine isolated ureteral smooth |
|
glandins on isolated human ureteric smooth muscle. Br |
|
|
muscle. J Urol. 2004;172:1155. |
|
J Urol. 1988;61:19-26. |
|
122
Practical Urology: EssEntial PrinciPlEs and PracticE
35.Mastrangelo D, Wisard M, Rohner S, Leisinger H, Iselin CE. Diclofenac and NS-398, a selective cyclooxygenase-2 inhibitor, decrease agonist-induced contractions of the pig isolated ureter. Urol Res. 2000;28:376-382.
36.Stief CG, Taher A, Truss M, Becker AJ, Schulz-Knapp P, et al. Phosphodiesterase isoenzymes in human ureteral smooth muscle: identification, characterization, and functional effects of various phosphodiesterase inhibitors in vitro. Urol Int. 1995;55:183-189.
37.Becker AJ, Stief CG, Meyer M, Truss M, Forssman WG. The effect of the specific phosphodiesterase-IV-inhibitor rolipram on the ureteral peristalsis of the rabbit in vitro and in vivo. J Urol. 1998;160:920-925.
38.Hertle L, Nawrath H. Calcium channel blockade in smooth muscle of the human upper urinary tract. II. Effects on norephinephrine-induced activation. J Urol. 1984;132:1270.
39.Hertle L, Nawrath H. Calcium channel blockade in smooth muscle of the human upper urinary tract. I. Effects on depolarization-induced activation. J Urol. 1984;132:1265.
40.Porpiglia F, Destenanis P, Fiori C, et al. Effectiveness of nifedipine and deflazacort in the management of distal ureter stones. Urology. 2000;56:579.
41.Caravati EM, Runge JW, Bossart RJ, et al. Nifedipine for the relief of renal colic: a double blind,placebo-controlled clinical trial. Ann Emerg Med. 1989; 18:352.
42.Yilmaz E, Batislam E, Bassar MM, Tuglu D, Ferhat M, et al. The comparison and efficacy of 3 different alpha1adrenergic blockers for distal ureteral stones. J Urol. 1005;173:2010-2012.
43.Dellabella M, Milanese G, Muzzonigro G. Efficacy of tamsulosin in the medical management of juxtavesical ureteral stones. J Urol. 2003;170:2202.
44.Dellabella M, Milanese G, Muzzonigro G. Randomized trial of the efficacy of tamsulosin, nifedipine and phloroglucinol in medical expulsive therapy for distal ureteral calculi. J Urol. 2005;174:167.
45.Dellabella M, Milanese G, Muzzonigro G. Medicalexpulsive therapy for distal ureterolithiasisi: randomized prospective study on role of corticosteroids used in compination with tamsulosin-simplified treatment regimen and health-related quality of life. Urology. 2005;666:712.
46.Hollingsworth JM, Rogers MA, Kaufman SR, Bradford TJ, Saint S. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet. 2006;368: 1171-1179.
47.Preminger GM, Tiselius HG, Assimos DG, Alken P, Buck C, Gallucci M. 2007 guideline for the management of ureteral calculi. J Urol. 2007;178:2418-2434.
48.Dellabella M, Milanese G, Muzzonigro G. Medicalexpulsive therapy for distal ureterolithiasis: randomized
prospective study on role of corticosteroids used in combination with tamsulosin-simplified treatment regimen and health-related quality of life. Urology. 2005;66:712-715.
49.Gravina GL, Costa AM, Ronchi P, Galatioto GP,Angelucci A, et al. Tamsulosin treatment increases clinical success rate of single extracorporeal shock wave lithotripsy of renal stones. Urology. 2005;66:24.
50.Resim S, Ekerbicer HC, CIftci A. Role of tamsulosin in treatment of patients with steinstrasse developing after extracorporeal shock wave lithotripsy. Urology. 2005;66:945.
51.Nakada SY, Hedican SP, Moon TD, Jerde TJ. Doxazosin relaxes ureteral smooth muscle and reverses epinephrine-induced ureteral contractility. J Urol. 2005;173(suppl):299. Abstract 1104.
52.Regoli D, Nguyen K, Calo G. Neurokinin receptors. Comparison of data from classical pharmacology, binding, and molecular biology. Ann NY Acad Sci. 1997;812:144-146.
53.Stief CG, Uckert S, Truss MC, Becker AJ, Machtens S, Jonas U. A possible role for nitric oxide in the regulation of human ureteral smooth muscle tone in vitro. Urol Res. 1996;24:333-337.
54.Iselin CE, Alm P, Schaad NC, Larsson B, Graber P, Anderson KE. Localization of nitric oxide synthase and haemoxygenase, and functional effects of nitric oxide and carbon monoxide in the pig and human intravesical ureter. Neururol Urodyn. 1997;16:209-227.
55.Yucel S, Baskin LS. Neuroanatomy of the ureterovesical junction: clinical implications. J Urol. 2003;170:945-948.
56.Venkatesh R, Landman J, Minor SD, Lee DI, Rehman J. Impact of a double-pigtail stent on ureteral peristalsis in the porcine model: initial studies using a novel implantable magnetic sensor. J Endourol. 2005;19:170-176.
57.Primbs K. Untersuchungen uber die Einwirkung von Bakterientoxinen auf der uberlebenden Meerschweinchenureter. Z Urol Chir. 1913;1:600.
58.Ross JA, Edmond P, Kirkland IS. Behavior of the Human Ureter in Health and Disease. Edinburgh, Scotland: Churchill Livingstone; 1972.
59.Akimoto M, Biancani P, Weiss RM. Comparative pres- sure-length-diameter relationships of neonatoal and adult rabbit ureters. Invest Urol. 1977;14:297.
60.Wheeler MA, Housman A, Cho YH, Weiss RM. Age dependence of adenylate cyclase activity in guinea pig ureter homogenate. J Pharmacol Exp Ther. 1986; 239:99.
61.Weiss RM. Physiology and pharmacology of the renal pelvis and ureter. In: Walsh PC, Retik AB, Vaughan ED, Wein A, eds. Campbell’s Urology. Philadelphia, PA: WB Saunders; 2008:1916-1917.