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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.
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http://dx.doi.org/10.14814/phy2.13899 | DOI Listing |
Kidney Int
November 2024
Molecular Biophysics, Saarland University, Homburg, Germany. Electronic address:
Onset, progression and cardiovascular outcome of chronic kidney disease (CKD) are influenced by the concomitant sterile inflammation. The pro-inflammatory cytokine family interleukin (IL)-1 is crucial in CKD with the key alarmin IL-1α playing an additional role as an adhesion molecule that facilitates immune cell tissue infiltration and consequently inflammation. Here, we investigate calcium ion and reactive oxygen species (ROS)-dependent regulation of different aspects of IL-1α-mediated inflammation.
View Article and Find Full Text PDFExp Neurol
February 2025
Department of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, Osaka, Japan; Core Research for Evolutional Science and Technology (CREST) from Japan Agency for Medical Research and Development (AMED), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Pharmacology, The Jikei University School of Medicine, Tokyo, Japan. Electronic address:
Intracranial aneurysms (IA) affect 1-5 % of the population and are a major cause of subarachnoid hemorrhage. Thus, preventing IA development and progression is crucial for public health. IA has been considered a non-physiological, high shear stress-induced chronic inflammatory disease affecting the bifurcation site of the intracranial arteries.
View Article and Find Full Text PDFF S Sci
October 2024
Division of Obstetrics and Gynecology, Tottori University Graduate School and Faculty of Medicine, Yonago, Tottori, Japan.
Objective: To evaluate the effects of a P2X4 receptor (P2X4R)-specific antagonist on murine endometriotic-like lesions and human endometriotic stromal cells.
Design: Experimental study using an in vivo mouse endometriosis model and in vitro primary culture of human endometriotic stromal cells. NC-2600, an antagonist of the P2X4 ionotropic ATP receptor (P2X4R), was orally administered to the mice and cells.
Front Immunol
October 2024
Hunan Provincial Key Laboratory of Traditional Chinese Medicine (TCM) Diagnostics, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Background: Linarine is a natural chemical component widely found in Buddleja officinalis Maxim., Chrysanthemum indicum L., Mentha canadensis L.
View Article and Find Full Text PDFJ Am Heart Assoc
October 2024
Department of Neurosciences School of Medicine, UConn Health Farmington CT USA.
Background: Purinergic receptor P2X4 (P2X4R), highly expressed on microglia and macrophages, is activated by ATP released from damaged cells and linked to poststroke inflammation. Previous studies showed that short-term P2X4R inhibition reduces inflammation and promotes long term recovery, but the mechanism underlying P2X4R and inflammation remains unclear. We hypothesized that P2X4R absence or pharmacological blockade can enhance macrophage phagocytic function by alleviating excessive inflammation after stroke.
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