Jens Georg Leipziger

The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice

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Standard

The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. / Craigie, Eilidh; Menzies, Robert I; Larsen, Casper K; Jacquillet, Grégory; Carrel, Monique; Wildman, Scott S; Loffing, Johannes; Leipziger, Jens; Shirley, David G; Bailey, Matthew A; Unwin, Robert J.

In: Physiological Reports, Vol. 6, No. 20, 22.10.2018, p. e13899.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Craigie, E, Menzies, RI, Larsen, CK, Jacquillet, G, Carrel, M, Wildman, SS, Loffing, J, Leipziger, J, Shirley, DG, Bailey, MA & Unwin, RJ 2018, 'The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice', Physiological Reports, vol. 6, no. 20, pp. e13899. https://doi.org/10.14814/phy2.13899

APA

Craigie, E., Menzies, R. I., Larsen, C. K., Jacquillet, G., Carrel, M., Wildman, S. S., Loffing, J., Leipziger, J., Shirley, D. G., Bailey, M. A., & Unwin, R. J. (2018). The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. Physiological Reports, 6(20), e13899. https://doi.org/10.14814/phy2.13899

CBE

Craigie E, Menzies RI, Larsen CK, Jacquillet G, Carrel M, Wildman SS, Loffing J, Leipziger J, Shirley DG, Bailey MA, Unwin RJ. 2018. The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. Physiological Reports. 6(20):e13899. https://doi.org/10.14814/phy2.13899

MLA

Vancouver

Craigie E, Menzies RI, Larsen CK, Jacquillet G, Carrel M, Wildman SS et al. The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. Physiological Reports. 2018 Oct 22;6(20):e13899. https://doi.org/10.14814/phy2.13899

Author

Craigie, Eilidh ; Menzies, Robert I ; Larsen, Casper K ; Jacquillet, Grégory ; Carrel, Monique ; Wildman, Scott S ; Loffing, Johannes ; Leipziger, Jens ; Shirley, David G ; Bailey, Matthew A ; Unwin, Robert J. / The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice. In: Physiological Reports. 2018 ; Vol. 6, No. 20. pp. e13899.

Bibtex

@article{186ce52bda5946db86169d267c248893,
title = "The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice",
abstract = "In the kidney, purinergic (P2) receptor-mediated ATP signaling has been shown to be an important local regulator of epithelial sodium transport. Appropriate sodium regulation is crucial for blood pressure (BP) control and disturbances in sodium balance can lead to hypo- or hypertension. Links have already been established between P2 receptor signaling and the development of hypertension, attributed mainly to vascular and/or inflammatory effects. A transgenic mouse model with deletion of the P2X4 receptor (P2X4-/- ) is known to have hypertension, which is thought to reflect endothelial dysfunction and impaired nitric oxide (NO) release. However, renal function in this model has not been characterized; moreover, studies in vitro have shown that the P2X4 receptor can regulate renal epithelial Na+ channel (ENaC) activity. Therefore, in the present study we investigated renal function and sodium handling in P2X4-/- mice, focusing on ENaC-mediated Na+ reabsorption. We confirmed an elevated BP in P2X4-/- mice compared with wild-type mice, but found that ENaC-mediated Na+ reabsorption is no different from wild-type and does not contribute to the raised BP observed in the knockout. However, when P2X4-/- mice were placed on a low sodium diet, BP normalized. Plasma aldosterone concentration tended to increase according to sodium restriction status in both genotypes; in contrast to wild-types, P2X4-/- mice did not show an increase in functional ENaC activity. Thus, although the increased BP in P2X4-/- mice has been attributed to endothelial dysfunction and impaired NO release, there is also a sodium-sensitive component.",
author = "Eilidh Craigie and Menzies, {Robert I} and Larsen, {Casper K} and Gr{\'e}gory Jacquillet and Monique Carrel and Wildman, {Scott S} and Johannes Loffing and Jens Leipziger and Shirley, {David G} and Bailey, {Matthew A} and Unwin, {Robert J}",
note = "{\textcopyright} 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.",
year = "2018",
month = oct,
day = "22",
doi = "10.14814/phy2.13899",
language = "English",
volume = "6",
pages = "e13899",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "20",

}

RIS

TY - JOUR

T1 - The renal and blood pressure response to low sodium diet in P2X4 receptor knockout mice

AU - Craigie, Eilidh

AU - Menzies, Robert I

AU - Larsen, Casper K

AU - Jacquillet, Grégory

AU - Carrel, Monique

AU - Wildman, Scott S

AU - Loffing, Johannes

AU - Leipziger, Jens

AU - Shirley, David G

AU - Bailey, Matthew A

AU - Unwin, Robert J

N1 - © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

PY - 2018/10/22

Y1 - 2018/10/22

N2 - In the kidney, purinergic (P2) receptor-mediated ATP signaling has been shown to be an important local regulator of epithelial sodium transport. Appropriate sodium regulation is crucial for blood pressure (BP) control and disturbances in sodium balance can lead to hypo- or hypertension. Links have already been established between P2 receptor signaling and the development of hypertension, attributed mainly to vascular and/or inflammatory effects. A transgenic mouse model with deletion of the P2X4 receptor (P2X4-/- ) is known to have hypertension, which is thought to reflect endothelial dysfunction and impaired nitric oxide (NO) release. However, renal function in this model has not been characterized; moreover, studies in vitro have shown that the P2X4 receptor can regulate renal epithelial Na+ channel (ENaC) activity. Therefore, in the present study we investigated renal function and sodium handling in P2X4-/- mice, focusing on ENaC-mediated Na+ reabsorption. We confirmed an elevated BP in P2X4-/- mice compared with wild-type mice, but found that ENaC-mediated Na+ reabsorption is no different from wild-type and does not contribute to the raised BP observed in the knockout. However, when P2X4-/- mice were placed on a low sodium diet, BP normalized. Plasma aldosterone concentration tended to increase according to sodium restriction status in both genotypes; in contrast to wild-types, P2X4-/- mice did not show an increase in functional ENaC activity. Thus, although the increased BP in P2X4-/- mice has been attributed to endothelial dysfunction and impaired NO release, there is also a sodium-sensitive component.

AB - In the kidney, purinergic (P2) receptor-mediated ATP signaling has been shown to be an important local regulator of epithelial sodium transport. Appropriate sodium regulation is crucial for blood pressure (BP) control and disturbances in sodium balance can lead to hypo- or hypertension. Links have already been established between P2 receptor signaling and the development of hypertension, attributed mainly to vascular and/or inflammatory effects. A transgenic mouse model with deletion of the P2X4 receptor (P2X4-/- ) is known to have hypertension, which is thought to reflect endothelial dysfunction and impaired nitric oxide (NO) release. However, renal function in this model has not been characterized; moreover, studies in vitro have shown that the P2X4 receptor can regulate renal epithelial Na+ channel (ENaC) activity. Therefore, in the present study we investigated renal function and sodium handling in P2X4-/- mice, focusing on ENaC-mediated Na+ reabsorption. We confirmed an elevated BP in P2X4-/- mice compared with wild-type mice, but found that ENaC-mediated Na+ reabsorption is no different from wild-type and does not contribute to the raised BP observed in the knockout. However, when P2X4-/- mice were placed on a low sodium diet, BP normalized. Plasma aldosterone concentration tended to increase according to sodium restriction status in both genotypes; in contrast to wild-types, P2X4-/- mice did not show an increase in functional ENaC activity. Thus, although the increased BP in P2X4-/- mice has been attributed to endothelial dysfunction and impaired NO release, there is also a sodium-sensitive component.

U2 - 10.14814/phy2.13899

DO - 10.14814/phy2.13899

M3 - Journal article

C2 - 30350402

VL - 6

SP - e13899

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 20

ER -