Fibroblast Growth Factor 2 Enhances Contraction of Arterioles in the Medulla Oblongata and the Basilar Artery in Mice With Chronic Kidney Disease.

Authors

Liang Zhao, Xingyu Qiu, Chunxiang Xu, Gensheng Zhang, Nan Xu, Pontus B Persson, Andreas Patzak, Jianhua Mao, En Yin Lai

Published in

Acta physiologica (Oxford, England). Volume 242. Issue 11. Pages e70327.

Abstract

Chronic kidney disease (CKD) augments vascular contractility in multiple vascular beds. Fibroblast growth factor 2 (FGF2), whose expression is upregulated in CKD, acts pro-contractile by supporting vasoconstrictor capacity. Thus, the present study tests whether CKD enhances cerebrovascular contractile responses to vasoconstrictors and a role of FGF2 in this setting.
We established CKD in mice by 5/6 nephrectomy and a 6% NaCl diet. Cerebrovascular reactivity was assessed in isolated brain basilar arteries and brain medulla oblongata arterioles using wire myography and microperfusion, respectively. Contractile responses to angiotensin II (Ang II), norepinephrine (NE), and endothelin-1 (ET-1) were measured. Expression of FGF2 and FGF binding protein 1 (FGFBP1) was assessed by immunohistochemistry, enzyme-linked immunosorbent assays, qPCR, and western blot. The role of the FGF2 pathway was evaluated using the selective FGFR tyrosine kinase inhibitor BGJ398.
Cerebrovascular contractile responses to Ang II, NE, and ET-1 were significantly enhanced in both the brain basilar artery and the brain medulla oblongata arterioles compared with the sham-operated group. FGF2 and FGFBP1 expression were upregulated in brain tissue after CKD, particularly in the medulla oblongata. Treatment with BGJ398 prevented the enhanced cerebrovascular contractile responses in CKD mice.
CKD enhances cerebrovascular contractile responses to vasoconstrictors, and this effect is mediated by activation of the FGF2 pathway. Targeting the FGF2 pathway may provide treatment of cerebrovascular dysfunction in CKD.

PMID:
42817617
Bibliographic data and abstract were imported from PubMed on 01 Oct 2026.

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