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- Stenqvist, Johanna, et al.
(författare)
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Urothelial acetylcholine involvement in ATP-induced contractile responses of the rat urinary bladder
- 2017
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Ingår i: European Journal of Pharmacology. - : Elsevier BV. - 0014-2999. ; 809, s. 253-260
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Tidskriftsartikel (refereegranskat)abstract
- Both acetylcholine and adenosine 5'-triphosphate (ATP) are released from the urothelium. In in vivo experiments ATP has been shown to evoke contractile responses that are significantly reduced by atropine. Currently, we aimed to examine the cholinergic part of the ATP-evoked contractile response of normal and inflamed (cyclophosphamide-treated rats) bladders. A whole bladder preparation that enabled drug administration either outside or inside the urinary bladder was used. The responses were examined in bladders from control and cyclophosphamide-treated rats that were either intact or urothelium-denuded. The expression of choline acetyltransferase and carnitine acetyltransferase were examined by Western blotting of normal and inflamed bladders. Methacholine evoked larger contractions when administered to the outside of the bladder in comparison to instillation. For ATP, an opposite trend emerged. While atropine substantially reduced the ATP-induced responses at internal administration (7.4 +/- 1.1 and 3.7 +/- 0.9 mN at 10-3 M; n=13; P < 0.001), it had no effect when administered outside the bladder. The removal of the urothelium caused a similar reduction of the responses to internal administration of ATP as caused by atropine. In cyclophosphamide-treated rats, neither atropine nor urothelium-denudation had any effect on the ATP-evoked responses. No changes in the expressions of the acetylcholine synthesising enzymes were observed. The current study shows that ATP induces a release of urothelial acetylcholine that contributes to the purinergic contractile response in the rat urinary bladder. This atropine-sensitive part of the purinergic contractile response is absent in the inflamed bladder. This may be one pathological mechanism involved in bladder dysfunction.
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- Winder, Michael, 1980, et al.
(författare)
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Autonomic Receptor-mediated Regulation of Production and Release of Nitric Oxide in Normal and Malignant Human Urothelial Cells
- 2017
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Ingår i: Basic & Clinical Pharmacology & Toxicology. - : Wiley. - 1742-7835. ; 121:4, s. 257-265
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Tidskriftsartikel (refereegranskat)abstract
- In the urinary bladder, the main source of NO seems to be the urothelium and the underlying suburothelium. In this study, we aimed to characterize how receptors in the human urothelium regulate the production and release of NO. For this, we cultured two human urothelial cell lines - the normal immortalized cell line UROtsa and the malignant cell line T24. These were treated with an array of agonists and antagonists with affinity for adrenergic, muscarinic and purinergic receptors. The production of NO and expression of nitric oxide synthase (NOS) was studied by immunocytochemistry and Western blotting. The amount of released NO was measured indirectly by detecting nitrite using amperometry and a Griess reaction kit. The results showed that NO, endothelial NOS and inducible NOS were predominantly produced and expressed in the close vicinity of the nucleus in untreated human urothelial cells. Upon treatment with a beta-adrenoceptor agonist, but not any of the other agonists or antagonists, the pattern of NO production changed, showing a more even production throughout the cytosol. The pattern of expression of endothelial NOS changed in a similar way upon dobutamine treatment. The release of nitrite, as a measurement of NO, increased after treatment with dobutamine from 0.31 +/- 0.029 to 1.97 +/- 0.18nmol and 0.80 +/- 0.12 to 3.27 +/- 0.24nmol in UROtsa and T24, respectively. In conclusion, our results show that the expression of NOS and production of NO as well as the release of NO from human urothelial cells is regulated by beta-adrenoceptor activation.
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- Winder, Monika, et al.
(författare)
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Increased appendicularian zooplankton alter carbon cycling under warmer more acidified ocean conditions
- 2017
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Ingår i: Limnology and Oceanography. - : John Wiley & Sons. - 0024-3590 .- 1939-5590. ; 62:4, s. 1541-1551
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Tidskriftsartikel (refereegranskat)abstract
- Anthropogenic atmospheric loading of CO2 raises concerns about combined effects of increasing ocean temperature and acidification, on biological processes. In particular, the response of appendicularian zooplankton to climate change may have significant ecosystem implications as they can alter biogeochemical cycling compared to classical copepod dominated food webs. However, the response of appendicularians to multiple climate drivers and effect on carbon cycling are still not well understood. Here, we investigated how gelatinous zooplankton (appendicularians) affect carbon cycling of marine food webs under conditions predicted by future climate scenarios. Appendicularians performed well in warmer conditions and benefited from low pH levels, which in turn altered the direction of carbon flow. Increased appendicularians removed particles from the water column that might otherwise nourish copepods by increasing carbon transport to depth from continuous discarding of filtration houses and fecal pellets. This helps to remove CO2 from the atmosphere, and may also have fisheries implications.
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