Chapter 1 : Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection

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The mammalian urinary tract is a contiguous hollow-organ system whose primary function is to collect, transport, store, and expel urine periodically and in a highly coordinated fashion ( ). In so doing, the urinary tract ensures the elimination of metabolic products and toxic wastes generated in the kidneys. The process of constant urine flow in the upper urinary tract and intermittent elimination from the lower urinary tract also plays a crucially important part in cleansing the urinary tract, ridding it of microbes that might have already gained access ( ). When not eliminating urine, the urinary tract acts effectively as a closed system, inaccessible to the microbes. Comprised, from proximal to distal, of renal papillae, renal pelvis, ureters, bladder, and urethra, each component of the urinary tract has distinct anatomic features and performs critical functions.

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012
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Figure 1

Normal anatomy of the kidney and upper urinary tract. (Reprinted from reference 163, with permission of the publisher.)

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012
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Figure 2

The ureterovesical junction. In this figure, A represents an orthotopic ureteral orifice. There is adequate length of ureteral tunnel in the bladder and therefore no reflux. Lateral and/or superior insertion of the ureteral orifice (B & C) can lead to inadequate submucosal ureter length and, potentially, reflux. (Reprinted from reference , with permission of the publisher.)

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012
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Figure 3

Assembly, intracelluar trafficking and structure of uroplakins. (a) Luminal portion of a superficial umbrella cell of mouse urothelium visualized by transmission electron microscopy (inset: an urothelial plaque exhibiting asymmetric unit membrane or AUM). (b) Quick-freeze deep-etch showing 16-nm uroplakin particles arranged in hexagonal arrays comprising the urothelial plaques (P) interconnected by particle-free hinges (H). (c) Vesicular trafficking in umbrella cells. Uroplakin heterodimer formation takes place in the endoplasmic reticulum (ER) and undergoes modification in the Golgi apparatus. Assembled uroplakins then amass in small vesicles and bud off the trans-Golgi network (TGN), forming discoidal vesicles (DVs). The next- stage, fusiform vesicles (FVs) pass through an intermediate-filament (IF) network and ultimately fuse with the apical membrane, a process mediated by Rab27b. Apical plaque-associated UPs are internalized via endocytic pathways and/or modified FVs that form sorting endosomes (SE) and multivesicular bodies (MVB), which merge with lysosomes (LYS) for degradation. (d) A hypothetical model of uroplakin assembly into 2-D crystals. Stages A and B: The four major uroplakins (UPIa, Ib, II, and IIIa) are modified with high-mannose glycans in the ER and hetero- dimerize forming UPIa/II and UPIb/IIIa and undergo major conformational changes. Symbols: the small, horizontal arrows on UPII denote the furin cleavage site at the end of the prosequence; the open and closed circles denote high-mannose and complex glycans, respectively. With urothelium (pathway on the right), the glycans on two of the three N-glycosylation sites on the prosequence of UPII become complex glycans in the TGN (stage C2), and the cleavage of the prosequence by furin in the TGN (stage D2) then triggers oligomerization to form a 16-nm particle. In cultured urothelial cells (pathway on the left), the differentiation-dependent glycosylation of pro-UPII is defective, preventing the formation of the uroplakin heterotetramer and the 16-nm particle, thus the lack of asymmetric-unit membrane. (Reprinted and adapted from reference , with permission of the publisher.)

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012
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Figure 4

Mechanism of storage and voiding. A. Storage of urine. Low-level bladder afferent firing, secondary to bladder distension, increases sympathetic outflow to the bladder outlet and external urethral sphincter (‘guarding reflex’). Sympathetic signaling also acts to inhibit detrusor-muscle contractions. B. Voiding. At bladder capacity, high-level bladder afferent activity activates the pontine-micturition center. This, in turn, inhibits the guarding reflex. The activated pontine-micturition center, under appropriate conditions, will lead to parasympathetic outflow to the bladder and internal-sphincter smooth muscle. Urinary sphincter relaxation is soon followed by a large, coordinated detrusor contraction leading to expulsion of urine from the bladder. (Reprinted and adapted from reference , with permission of the publisher.)

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012
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Anatomic causes of ureteral obstruction

Citation: Hickling D, Sun T, Wu X. 2017. Anatomy and Physiology of the Urinary Tract: Relation to Host Defense and Microbial Infection, p 3-25. In Mulvey M, Klumpp D, Stapleton A (ed), Urinary Tract Infections: Molecular Pathogenesis and Clinical Management, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.UTI-0016-2012

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