Aldosterone stimulates active Na+ transport in rabbit urinary bladder by both genomic and non-genomic processes

Burton, Timothy J.; Cooper, Dermot M.F.; Dunning-Davies, Bryony; Mansour, Dina; Masada, Nanako; Ferguson, D. R.

doi:10.1016/j.ejphar.2005.01.017

Cited by 6 publications

(3 citation statements)

References 13 publications

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“…Moreover, the hypotonic induction of SGK did not require the activity of RTK or JNK/SAPK, and inhibition of RTK did not affect the increase in Na ϩ transport by overnight reduction in extracellular osmolality (Taruno A, unpublished observations). The data strongly suggest that, like aldosterone (7,10,52), hypotonic stress has both genomic and nongenomic effects on Na ϩ transport and that the RTK-JNK/SAPK cascade mediates nongenomic stimulation constituting the early phase of the hypotonic action on Na ϩ transport.…”

Section: Discussionmentioning

confidence: 95%

Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases

Taruno

Niisato²,

Marunaka³

2007

American Journal of Physiology-Renal Physiology

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We previously reported that hypotonic stress stimulated transepithelial Na(+) transport via a pathway dependent on protein tyrosine kinase (PTK; Niisato N, Van Driessche W, Liu M, Marunaka Y. J Membr Biol 175: 63-77, 2000). However, it is still unknown what type of PTK mediates this stimulation. In the present study, we investigated the role of receptor tyrosine kinase (RTK) in the hypotonic stimulation of Na(+) transport. In renal epithelial A6 cells, we observed inhibitory effects of AG1478 [an inhibitor of the EGF receptor (EGFR)] and AG1296 [an inhibitor of the PDGF receptor (PDGFR)] on both the hypotonic stress-induced stimulation of Na(+) transport and the hypotonic stress-induced ligand-independent activation of EGFR. We further studied whether hypotonic stress activates members of the MAP kinase family, ERK1/2, p38 MAPK, and JNK/SAPK, via an RTK-dependent pathway. The present study indicates that hypotonic stress induced phosphorylation of ERK1/2 and JNK/SAPK, but not p38 MAPK, that the hypotonic stress-induced phosphorylation of ERK1/2 and JNK/SAPK was diminished by coapplication of AG1478 and AG1296, and that only JNK/SAPK was involved in the hypotonic stimulation of Na(+) transport. A further study using cyclohexamide (a protein synthesis inhibitor) suggests that both RTK and JNK/SAPK contributed to the protein synthesis-independent early phase in hypotonic stress-induced Na(+) transport, but not to the protein synthesis-dependent late phase. The present study also suggests involvement of phosphatidylinositol 3-kinase (PI3-kinase) in RTK-JNK/SAPK cascade-mediated Na(+) transport. These observations indicate that 1) hypotonic stress activates JNK/SAPK via RTKs in a ligand-independent pathway, 2) the RTK-JNK/SAPK cascade acts as a mediator of hypotonic stress for stimulation of Na(+) transport, and 3) PI3-kinase is involved in the RTK-JNK/SAPK cascade for the hypotonic stress-induced stimulation of Na(+) transport.

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Section: Discussionmentioning

confidence: 95%

Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases

Taruno

Niisato²,

Marunaka³

2007

American Journal of Physiology-Renal Physiology

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“…Yet, it has been known for several decades that the bladder, renal pelvis, and ureters have the potential to modify urine via transport of Na + , K + , urea, water, and creatinine across the urothelium . Furthermore, the Na + ‐conserving hormone, aldosterone, increases Na + transport across the bladder wall and anti‐diuretic hormone (ADH) induces net movement of water across the frog bladder wall …”

Section: Introductionmentioning

confidence: 99%

“…Yet, it has been known for several decades that the bladder, renal pelvis, 7 and ureters 8 have the potential to modify urine via transport of Na + , K + , urea, water, and creatinine across the urothelium. 9 Furthermore, the Na + -conserving hormone, aldosterone, increases Na + transport across the bladder wall 10 and anti-diuretic hormone (ADH) induces net movement of water across the frog bladder wall. 11 The aim of the present article is to review what is known of urine modification in the urinary tract and to highlight areas of research needed to advance our understanding of this area within a clinically relevant context.…”

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confidence: 99%

Is electrolyte transfer across the urothelium important?: ICI‐RS 2015

McCloskey

Vahabi

Fry

2017

Neurourology and Urodynamics

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Is the urothelium intelligent?

Birder

Cruz

Moore

et al. 2010

Neurourology and Urodynamics

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The urothelium separates the urinary tract lumen from underlying tissues of the tract wall. Previously considered as merely an effective barrier between these two compartments it is now recognized as a more active tissue that senses and transduces information about physical and chemical conditions within the urinary tract, such as luminal pressure, urine composition, etc. To understand this sensory function it is useful to consider the urothelium and suburothelium as a functional unit; containing uroepithelial cells, afferent and efferent nerve fibers and suburothelial interstitial cells. This structure responds to alterations in its external environment through the release of diffusible agents, such as ATP and acetylcholine, and eventually modulates the activity of afferent nerves and underlying smooth muscles. This review considers different stresses the urothelium/suburothelium responds to; the particular chemicals released; the cellular receptors that are consequently affected; and how nerve and muscle function is modulated. Brief consideration is also to regional differences in the urothelium/suburothelium along the urinary tract. The importance of different pathways in relaying sensory information in the normal urinary tract, or whether they are significant only in pathological conditions is also discussed. An operational definition of intelligence is used, whereby a system (urothelium/suburothelium) responds to external changes, to maximize the possibility of the urinary tract achieving its normal function. If so, the urothelium can be regarded as intelligent. The advantage of this approach is that input–output functions can be mathematically formulated, and the importance of different components contributing to abnormal urinary tract function can be calculated.

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Aldosterone stimulates active Na+ transport in rabbit urinary bladder by both genomic and non-genomic processes

Cited by 6 publications

References 13 publications

Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases

Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases

Is electrolyte transfer across the urothelium important?: ICI‐RS 2015

Is the urothelium intelligent?

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