Endothelin in the Urinary Bladder. I. Synthesis of Endothelin-1 by Epithelia, Smooth Muscle and Fibroblasts Suggests Autocrine and Paracrine Cellular Regulation

Tejada, Iñigo Sáenz de; Mueller, James; Morenas, Antonio de las; Machado, Michelle; Moreland, Robert B.; Krane, Robert J.; Wolfe, Hubert J.; Traish, Abdulmaged M.

doi:10.1016/s0022-5347(17)36895-7

Cited by 59 publications

(39 citation statements)

References 36 publications

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“…The highest density of binding sites appeared to be in vessels and the outer muscle layer. Saenz de Tejada et al (1992) demonstrated ET-like immunoreactivity in the transitional epithelium, serosal mesothelium, vascular endothelium, smooth muscles of the detrusor and vessels, and in fibroblasts in both human and rabbit bladder. This cellular distribution was confirmed in in situ hybridization experiments.…”

Section: Peripheral Targetsmentioning

confidence: 95%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

455

364

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Section: Peripheral Targetsmentioning

confidence: 95%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

455

364

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“…Saenz de Tejada et al 87 suggested that ETs may act as an autocrine hormone in the regulation of bladder wall structure and smooth muscle tone, and that it may regulate cholinergic neurotransmission by a paracrine mechanism. The contractile effect of ETs seems to be mediated mainly by the ET A receptor.…”

Section: Local Mediators Influencing Spontaneous Activitymentioning

confidence: 99%

Detrusor myocyte activity and afferent signaling

Andersson

2009

Neurourology and Urodynamics

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Aims: To discuss (1) mechanisms involved in the generation and control of myocyte contractions and consequent afferent nerve activity and (2) these mechanisms as targets for drugs aimed for treatment of overactive bladder (OAB) symptoms and detrusor overactivity (DO). Methods: Literature review of myocyte activation, bladder afferent nerves, mediators in the bladder, and translational aspects of the findings. Results: During bladder filling, there is normally no parasympathetic outflow from the spinal cord. Despite this, the bladder develops tone during filling and also exhibits non-synchronized local contractions and relaxations that are caused by a basal myogenic mechanical activity that may be reinforced by release of, for example, acetylcholine from non-neuronal and/or neuronal sources or local mediators, such as prostaglandins and endothelins. It is suggested that these spontaneous contractions are able to generate activity in afferent nerves (''afferent noise'') that may contribute to DO and OAB. Conclusions: Spontaneous bladder myocyte contractions and factors that are able to modulate them, as well as the consequent afferent nerve activity, may be targets for drugs meant for treatment of OAB/DO. Neurourol.

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“…ET-1 is synthesized by both vascular and non-vascular smooth muscle cells (2). In addition to producing potent contractions in vascular smooth muscle, ET-1 can also produce contractions in other non-vascular smooth muscles including the urinary bladder from a number of species (3 -8).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…ET-like immunoreactivity and [ 125 I] ET-1 binding sites were identified in detrusor smooth muscles, epithelia, and vascular endothelium (2,15). ET-1 is synthesized not only by smooth muscle cells in the urinary bladder, but also by epithelial cells and fibroblasts (2). Furthermore, the intravenous infusion of ET-1 was shown to cause a decrease in the mean micturition volume of rats in addition to an increase in mean arterial pressure (16 effects on various urinary dysfunctions including benign prostatic hyperplasia (17).…”

Section: Introductionmentioning

confidence: 99%

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