Adenosine Triphosphate

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Mervyn Singer - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of vascular Adenosine Triphosphate-sensitive potassium channels by sympathetic tone during sepsis.
    Critical care medicine, 2012
    Co-Authors: Yi-ling Chan, Nelson N. Orie, Alex Dyson, Valerie Taylor, Raymond Stidwill, Lucie H. Clapp, Mervyn Singer
    Abstract:

    OBJECTIVE Excessive opening of the Adenosine Triphosphate-sensitive potassium channel in vascular smooth muscle is implicated in the vasodilation and vascular hyporeactivity underlying septic shock. Therapeutic channel inhibition using sulfonylurea agents has proved disappointing, although agents acting on its pore appear more promising. We thus investigated the hemodynamic effects of Adenosine Triphosphate-sensitive potassium channel pore inhibition in awake, fluid-resuscitated septic rats, and the extent to which these responses are modulated by the high sympathetic tone present in sepsis. Temporal changes in ex-vivo channel activity and subunit gene expression were also investigated. DESIGN In vivo and ex vivo animal study. SETTING University research laboratory. SUBJECTS Male adult Wistar rats. INTERVENTIONS AND MEASUREMENTS Fecal peritonitis was induced in conscious, fluid-resuscitated rats. Pressor responses to norepinephrine and PNU-37883A (a vascular Adenosine Triphosphate-sensitive potassium channel inhibitor acting on the Kir6.1 pore-forming subunit) were measured at 6 or 24 hrs, in the absence or presence of the autonomic ganglion blocker, pentolinium. The aorta and mesenteric artery were examined ex vivo for rubidium efflux as a marker of Adenosine Triphosphate-sensitive potassium channel activity, and for Adenosine Triphosphate-sensitive potassium channel subunit gene expression using quantitative reverse transcription-polymerase chain reaction. MAIN RESULTS A total of 120 rats (50 sham-operated controls, 70 septic) were included. Septic rats became hypotensive after 12 hrs, with a 24-hr mortality of 51.7% (0% in controls). At 6 hrs, there was an attenuated pressor response to norepinephrine (p < .01) despite blood pressure being elevated (p < .01). PNU-37883A had no pressor effect, except in the presence of pentolinium (p < .01). Kir6.1 subunit mRNA increased significantly in the mesenteric artery while rubidium efflux was increased in both the aorta and mesenteric artery at 24 hrs. CONCLUSIONS Despite evidence of increased Adenosine Triphosphate-sensitive potassium channel activity in sepsis, it appears to be inhibited in vivo by high sympathetic tone. This may explain, at least in part, the reduced efficacy of Adenosine Triphosphate-sensitive potassium channel blockers in human septic shock.

J Ganowicz - One of the best experts on this subject based on the ideXlab platform.

Seiji Naito - One of the best experts on this subject based on the ideXlab platform.

  • Diphosphate Regulation of Adenosine Triphosphate Sensitive Potassium Channel in Human Bladder Smooth Muscle Cells
    The Journal of urology, 2011
    Co-Authors: Shunichi Kajioka, Nouval Shahab, Haruhiko Asano, Hiromitsu Morita, Megumi Sugihara, Fumi Takahashi-yanaga, Tatsuya Yoshihara, Shinsuke Nakayama, Narihito Seki, Seiji Naito
    Abstract:

    Purpose: To clarify the properties of Adenosine Triphosphate sensitive K+ channel in human detrusor smooth muscle we examined the effect of the representative nicotinic acid derivatives β-nicotinamide adenine dinucleotide, cyclic Adenosine diphosphate ribose and nicotinic acid adenine dinucleotide phosphate (Sigma-Aldrich®) on human detrusor Adenosine Triphosphate sensitive K+ channels.Materials and Methods: Patch clamp procedures were done in human detrusor cells. Reverse transcriptase and real-time polymerase chain reaction were performed to clarify the subunit components of Adenosine Triphosphate sensitive K+ channels.Results: The K+ channel opener levcromakalim induced a long lasting outward current that was inhibited by glibenclamide (Sigma-Aldrich) under the whole cell configuration. The single channel study revealed that the unitary conductance of the Adenosine Triphosphate sensitive K+ channel in the human detrusor was 11 pS and nucleotide diphosphates increased its open probability. Applying β-ni...

Yi-ling Chan - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of vascular Adenosine Triphosphate-sensitive potassium channels by sympathetic tone during sepsis.
    Critical care medicine, 2012
    Co-Authors: Yi-ling Chan, Nelson N. Orie, Alex Dyson, Valerie Taylor, Raymond Stidwill, Lucie H. Clapp, Mervyn Singer
    Abstract:

    OBJECTIVE Excessive opening of the Adenosine Triphosphate-sensitive potassium channel in vascular smooth muscle is implicated in the vasodilation and vascular hyporeactivity underlying septic shock. Therapeutic channel inhibition using sulfonylurea agents has proved disappointing, although agents acting on its pore appear more promising. We thus investigated the hemodynamic effects of Adenosine Triphosphate-sensitive potassium channel pore inhibition in awake, fluid-resuscitated septic rats, and the extent to which these responses are modulated by the high sympathetic tone present in sepsis. Temporal changes in ex-vivo channel activity and subunit gene expression were also investigated. DESIGN In vivo and ex vivo animal study. SETTING University research laboratory. SUBJECTS Male adult Wistar rats. INTERVENTIONS AND MEASUREMENTS Fecal peritonitis was induced in conscious, fluid-resuscitated rats. Pressor responses to norepinephrine and PNU-37883A (a vascular Adenosine Triphosphate-sensitive potassium channel inhibitor acting on the Kir6.1 pore-forming subunit) were measured at 6 or 24 hrs, in the absence or presence of the autonomic ganglion blocker, pentolinium. The aorta and mesenteric artery were examined ex vivo for rubidium efflux as a marker of Adenosine Triphosphate-sensitive potassium channel activity, and for Adenosine Triphosphate-sensitive potassium channel subunit gene expression using quantitative reverse transcription-polymerase chain reaction. MAIN RESULTS A total of 120 rats (50 sham-operated controls, 70 septic) were included. Septic rats became hypotensive after 12 hrs, with a 24-hr mortality of 51.7% (0% in controls). At 6 hrs, there was an attenuated pressor response to norepinephrine (p < .01) despite blood pressure being elevated (p < .01). PNU-37883A had no pressor effect, except in the presence of pentolinium (p < .01). Kir6.1 subunit mRNA increased significantly in the mesenteric artery while rubidium efflux was increased in both the aorta and mesenteric artery at 24 hrs. CONCLUSIONS Despite evidence of increased Adenosine Triphosphate-sensitive potassium channel activity in sepsis, it appears to be inhibited in vivo by high sympathetic tone. This may explain, at least in part, the reduced efficacy of Adenosine Triphosphate-sensitive potassium channel blockers in human septic shock.

Christopher R Chapple - One of the best experts on this subject based on the ideXlab platform.

  • enhanced Adenosine Triphosphate release from the urothelium of patients with painful bladder syndrome a possible pathophysiological explanation
    The Journal of Urology, 2007
    Co-Authors: Vivek Kumar, Christopher R Chapple, Ann Marie Surprenant, Russ Chesswilliams
    Abstract:

    Purpose: We established the level of Adenosine Triphosphate release by the urothelium in patients with painful bladder syndrome and compared it with that from the normal human bladder.Materials and Methods: Biopsies of urothelium from patients with painful bladder syndrome were subjected to stretch by 130% and 150% of the original length, and 10 Hz electric stimulation. A luciferase assay was used to quantify Adenosine Triphosphate release. The neurotoxin tetrodotoxin was used to block the neuronal source of Adenosine Triphosphate release.Results: There was a significantly greater release of Adenosine Triphosphate following mechanical stretch of the urothelium from painful vs control bladders. The increase in Adenosine Triphosphate release in painful vs control bladders was statistically significant whether expressed in absolute values (mean ± SE 3,791.4 ± 667.9 vs 77.6 ± 16.2 pM gm−1 tissue) or as an increase over baseline (282.2% ± 24.8% vs 175.4% ± 21.7%). Similarly there was a significant release of a...

  • Enhanced Adenosine Triphosphate release from the urothelium of patients with painful bladder syndrome: a possible pathophysiological explanation.
    The Journal of urology, 2007
    Co-Authors: Vivek Kumar, Christopher R Chapple, Ann Marie Surprenant, Russell Chess-williams
    Abstract:

    We established the level of Adenosine Triphosphate release by the urothelium in patients with painful bladder syndrome and compared it with that from the normal human bladder. Biopsies of urothelium from patients with painful bladder syndrome were subjected to stretch by 130% and 150% of the original length, and 10 Hz electric stimulation. A luciferase assay was used to quantify Adenosine Triphosphate release. The neurotoxin tetrodotoxin was used to block the neuronal source of Adenosine Triphosphate release. There was a significantly greater release of Adenosine Triphosphate following mechanical stretch of the urothelium from painful vs control bladders. The increase in Adenosine Triphosphate release in painful vs control bladders was statistically significant whether expressed in absolute values (mean +/- SE 3,791.4 +/- 667.9 vs 77.6 +/- 16.2 pM gm(-1) tissue) or as an increase over baseline (282.2% +/- 24.8% vs 175.4% +/- 21.7%). Similarly there was a significant release of Adenosine Triphosphate following electrical field stimulation of the urothelium from painful vs control bladders (1,348.6 +/- 278.2 vs 61.7 +/- 10.1 pM gm(-1) tissue, p <0.005), representing a 278% +/- 41.5% vs 137.9% +/- 4.4% increase above baseline (p <0.005). The source of Adenosine Triphosphate release was nonneuronal in 89% of painful bladders and in 84% of control bladders. There is a significantly increased level of Adenosine Triphosphate release from the urothelium of painful bladders in comparison to that from normal bladders, suggesting an important potential functional role for Adenosine Triphosphate in this condition.