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Novel role of AQP-1 in NO-dependent vasorelaxation

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Zeitschriftentitel: American Journal of Physiology-Renal Physiology
Personen und Körperschaften: Herrera, Marcela, Garvin, Jeffrey L.
In: American Journal of Physiology-Renal Physiology, 292, 2007, 5, S. F1443-F1451
Medientyp: E-Article
Sprache: Englisch
veröffentlicht:
American Physiological Society
Schlagwörter:
author_facet Herrera, Marcela
Garvin, Jeffrey L.
Herrera, Marcela
Garvin, Jeffrey L.
author Herrera, Marcela
Garvin, Jeffrey L.
spellingShingle Herrera, Marcela
Garvin, Jeffrey L.
American Journal of Physiology-Renal Physiology
Novel role of AQP-1 in NO-dependent vasorelaxation
Physiology
author_sort herrera, marcela
spelling Herrera, Marcela Garvin, Jeffrey L. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00353.2006 <jats:p>Nitric oxide (NO) produced by endothelial cells diffuses to vascular smooth muscle cells to cause dilatation of the renal vasculature and other vessels. Although it is generally assumed that NO moves from cell to cell by free diffusion, we recently showed that aquaporin-1 (AQP-1) transports NO across cell membranes. AQP-1 is expressed in endothelial and vascular smooth muscle cells. We hypothesized that diffusion of NO into vascular smooth muscle cells and out of endothelial cells is facilitated by AQP-1, and transport of NO by AQP-1 is involved in endothelium-dependent relaxation. In intact aortic rings from AQP-1 −/− mice, vasorelaxation induced by acetylcholine (which increases endogenous NO) was reduced ( P &lt; 0.0001 vs. control). No differences were found in the relaxation caused by intracellular delivery of NO or intracellular cGMP between strains. In endothelium-denuded aortic rings from AQP-1 −/− mice, the vasorelaxant capability of NO released in the extracellular space was reduced ( P &lt; 0.0001 vs. control). Influx of NO (5 μM) into vascular smooth muscle cells was 0.17 ± 0.02 f.u./s for control and 0.07 ± 0.01 f.u./s for AQP-1 −/− mice, 62% lower ( P &lt; 0.002). NO released by endothelial cells in response to 1 μM acetylcholine was 96.2 ± 17.7 pmol NO/mg for control and 41.9 ± 13.4 pmol NO/mg for AQP-1 −/− mice, 56% reduction ( P &lt; 0.04). NOS3 expression was 1.33 ± 0.29 O.D. units for control and 3.84 ± 0.76 O.D. units for AQP-1 −/− mice, 188% increase ( P &lt; 0.01). We conclude that 1) AQP-1 facilitates NO influx into vascular smooth muscle cells, 2) AQP-1 facilitates NO diffusion out of endothelial cells, and 3) transport of NO by AQP-1 is required for full expression of endothelium-dependent relaxation.</jats:p> Novel role of AQP-1 in NO-dependent vasorelaxation American Journal of Physiology-Renal Physiology
doi_str_mv 10.1152/ajprenal.00353.2006
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title Novel role of AQP-1 in NO-dependent vasorelaxation
title_unstemmed Novel role of AQP-1 in NO-dependent vasorelaxation
title_full Novel role of AQP-1 in NO-dependent vasorelaxation
title_fullStr Novel role of AQP-1 in NO-dependent vasorelaxation
title_full_unstemmed Novel role of AQP-1 in NO-dependent vasorelaxation
title_short Novel role of AQP-1 in NO-dependent vasorelaxation
title_sort novel role of aqp-1 in no-dependent vasorelaxation
topic Physiology
url http://dx.doi.org/10.1152/ajprenal.00353.2006
publishDate 2007
physical F1443-F1451
description <jats:p>Nitric oxide (NO) produced by endothelial cells diffuses to vascular smooth muscle cells to cause dilatation of the renal vasculature and other vessels. Although it is generally assumed that NO moves from cell to cell by free diffusion, we recently showed that aquaporin-1 (AQP-1) transports NO across cell membranes. AQP-1 is expressed in endothelial and vascular smooth muscle cells. We hypothesized that diffusion of NO into vascular smooth muscle cells and out of endothelial cells is facilitated by AQP-1, and transport of NO by AQP-1 is involved in endothelium-dependent relaxation. In intact aortic rings from AQP-1 −/− mice, vasorelaxation induced by acetylcholine (which increases endogenous NO) was reduced ( P &lt; 0.0001 vs. control). No differences were found in the relaxation caused by intracellular delivery of NO or intracellular cGMP between strains. In endothelium-denuded aortic rings from AQP-1 −/− mice, the vasorelaxant capability of NO released in the extracellular space was reduced ( P &lt; 0.0001 vs. control). Influx of NO (5 μM) into vascular smooth muscle cells was 0.17 ± 0.02 f.u./s for control and 0.07 ± 0.01 f.u./s for AQP-1 −/− mice, 62% lower ( P &lt; 0.002). NO released by endothelial cells in response to 1 μM acetylcholine was 96.2 ± 17.7 pmol NO/mg for control and 41.9 ± 13.4 pmol NO/mg for AQP-1 −/− mice, 56% reduction ( P &lt; 0.04). NOS3 expression was 1.33 ± 0.29 O.D. units for control and 3.84 ± 0.76 O.D. units for AQP-1 −/− mice, 188% increase ( P &lt; 0.01). We conclude that 1) AQP-1 facilitates NO influx into vascular smooth muscle cells, 2) AQP-1 facilitates NO diffusion out of endothelial cells, and 3) transport of NO by AQP-1 is required for full expression of endothelium-dependent relaxation.</jats:p>
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author Herrera, Marcela, Garvin, Jeffrey L.
author_facet Herrera, Marcela, Garvin, Jeffrey L., Herrera, Marcela, Garvin, Jeffrey L.
author_sort herrera, marcela
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description <jats:p>Nitric oxide (NO) produced by endothelial cells diffuses to vascular smooth muscle cells to cause dilatation of the renal vasculature and other vessels. Although it is generally assumed that NO moves from cell to cell by free diffusion, we recently showed that aquaporin-1 (AQP-1) transports NO across cell membranes. AQP-1 is expressed in endothelial and vascular smooth muscle cells. We hypothesized that diffusion of NO into vascular smooth muscle cells and out of endothelial cells is facilitated by AQP-1, and transport of NO by AQP-1 is involved in endothelium-dependent relaxation. In intact aortic rings from AQP-1 −/− mice, vasorelaxation induced by acetylcholine (which increases endogenous NO) was reduced ( P &lt; 0.0001 vs. control). No differences were found in the relaxation caused by intracellular delivery of NO or intracellular cGMP between strains. In endothelium-denuded aortic rings from AQP-1 −/− mice, the vasorelaxant capability of NO released in the extracellular space was reduced ( P &lt; 0.0001 vs. control). Influx of NO (5 μM) into vascular smooth muscle cells was 0.17 ± 0.02 f.u./s for control and 0.07 ± 0.01 f.u./s for AQP-1 −/− mice, 62% lower ( P &lt; 0.002). NO released by endothelial cells in response to 1 μM acetylcholine was 96.2 ± 17.7 pmol NO/mg for control and 41.9 ± 13.4 pmol NO/mg for AQP-1 −/− mice, 56% reduction ( P &lt; 0.04). NOS3 expression was 1.33 ± 0.29 O.D. units for control and 3.84 ± 0.76 O.D. units for AQP-1 −/− mice, 188% increase ( P &lt; 0.01). We conclude that 1) AQP-1 facilitates NO influx into vascular smooth muscle cells, 2) AQP-1 facilitates NO diffusion out of endothelial cells, and 3) transport of NO by AQP-1 is required for full expression of endothelium-dependent relaxation.</jats:p>
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spelling Herrera, Marcela Garvin, Jeffrey L. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00353.2006 <jats:p>Nitric oxide (NO) produced by endothelial cells diffuses to vascular smooth muscle cells to cause dilatation of the renal vasculature and other vessels. Although it is generally assumed that NO moves from cell to cell by free diffusion, we recently showed that aquaporin-1 (AQP-1) transports NO across cell membranes. AQP-1 is expressed in endothelial and vascular smooth muscle cells. We hypothesized that diffusion of NO into vascular smooth muscle cells and out of endothelial cells is facilitated by AQP-1, and transport of NO by AQP-1 is involved in endothelium-dependent relaxation. In intact aortic rings from AQP-1 −/− mice, vasorelaxation induced by acetylcholine (which increases endogenous NO) was reduced ( P &lt; 0.0001 vs. control). No differences were found in the relaxation caused by intracellular delivery of NO or intracellular cGMP between strains. In endothelium-denuded aortic rings from AQP-1 −/− mice, the vasorelaxant capability of NO released in the extracellular space was reduced ( P &lt; 0.0001 vs. control). Influx of NO (5 μM) into vascular smooth muscle cells was 0.17 ± 0.02 f.u./s for control and 0.07 ± 0.01 f.u./s for AQP-1 −/− mice, 62% lower ( P &lt; 0.002). NO released by endothelial cells in response to 1 μM acetylcholine was 96.2 ± 17.7 pmol NO/mg for control and 41.9 ± 13.4 pmol NO/mg for AQP-1 −/− mice, 56% reduction ( P &lt; 0.04). NOS3 expression was 1.33 ± 0.29 O.D. units for control and 3.84 ± 0.76 O.D. units for AQP-1 −/− mice, 188% increase ( P &lt; 0.01). We conclude that 1) AQP-1 facilitates NO influx into vascular smooth muscle cells, 2) AQP-1 facilitates NO diffusion out of endothelial cells, and 3) transport of NO by AQP-1 is required for full expression of endothelium-dependent relaxation.</jats:p> Novel role of AQP-1 in NO-dependent vasorelaxation American Journal of Physiology-Renal Physiology
spellingShingle Herrera, Marcela, Garvin, Jeffrey L., American Journal of Physiology-Renal Physiology, Novel role of AQP-1 in NO-dependent vasorelaxation, Physiology
title Novel role of AQP-1 in NO-dependent vasorelaxation
title_full Novel role of AQP-1 in NO-dependent vasorelaxation
title_fullStr Novel role of AQP-1 in NO-dependent vasorelaxation
title_full_unstemmed Novel role of AQP-1 in NO-dependent vasorelaxation
title_short Novel role of AQP-1 in NO-dependent vasorelaxation
title_sort novel role of aqp-1 in no-dependent vasorelaxation
title_unstemmed Novel role of AQP-1 in NO-dependent vasorelaxation
topic Physiology
url http://dx.doi.org/10.1152/ajprenal.00353.2006