ArticleHypertension research : official journal of the Japanese Society of Hypertension2017
Increased blood pressure in nesfatin/nuclebindin-2-transgenic mice.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 15 citations in OpenAlex.
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- The role of nesfatin-1 in kidney diseases.Pediatric nephrology (Berlin, Germany) · 2025Review
- Nesfatin-1 enhances vascular smooth muscle calcification through facilitating BMP-2 osteogenic signaling.Cell communication and signaling : CCS · 2024Article
- Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension.iScience · 2024Article
- Role of the Novel Peptide Phoenixin in Stress Response and Possible Interactions with Nesfatin-1.International journal of molecular sciences · 2021Review
- Nesfatin-1 suppresses peripheral arterial remodeling without elevating blood pressure in mice.Endocrine connections · 2019Article
- Current Understanding of the Role of Nesfatin-1.Journal of the Endocrine Society · 2018Review
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
Nesfatin/nucleobindin-2 (nesf/NUCB2), a precursor of the anorexigenic protein nesfatin-1, is selectively expressed in the hypothalamic nuclei, which are central to the regulation of the autonomic nervous system. The present study sought to investigate the involvement of nesf/NUCB2 in the regulation of blood pressure and ingestive behavior, by using nesf/NUCB2-transgenic (Tg) mice. Blood pressure and heart rates were measured under conscious and unconscious conditions. Twenty-four-hour water intake and urine volume of male nesf/NUCB2-Tg mice and their littermates in metabolic cages were measured. After killing, kidney weight was measured and the mRNA expression of epithelial sodium channel (ENaC)-α and ENaC-γ was measured in the hypothalamus and kidney with real-time PCR. Systolic, diastolic and mean blood pressure were significantly higher in nesf/NUCB2-Tg mice, but pulse rate was not affected in conscious mice. In contrast, isoflurane anesthesia prevented an increase in blood pressure in the nesf/NUCB2-Tg mice. Twenty-four-hour water intake and urine volume were significantly higher in the nesf/NUCB2-Tg mice than in their non-Tg littermates. Urine sodium concentration was significantly lower in the nesf/NUCB2-Tg mice, although the serum sodium concentration and urine sodium excretion were not different between the genotypes. Kidney weight was significantly higher in the nesf/NUCB2-Tg mice than their non-Tg littermates, although there were no clear differences in the kidney histological findings between genotypes. The mRNA expression of ENaC-γ, but not ENaC-α, was decreased in the hypothalami of nesf/NUCB2-Tg mice. Our data suggested that Nesf/NUCB2 is involved in the regulation of blood pressure in the brain.
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