Increased blood pressure in nesfatin/nuclebindin-2-transgenic mice
Yusaku Mori1, Hiroyuki Shimizu2, Hideki Kushima1
1Division of Diabetes, Metabolism and Endocrinology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Summary
Nesfatin/nucleobindin-2 (nesf/NUCB2) influences blood pressure regulation in the brain. Transgenic mice showed higher blood pressure and water intake, suggesting nesf/NUCB2
Area of Science:
- Neuroendocrinology
- Cardiovascular Physiology
- Renal Physiology
Background:
- Nesfatin/nucleobindin-2 (nesf/NUCB2) is a precursor to the anorexigenic protein nesfatin-1.
- nesf/NUCB2 is expressed in hypothalamic nuclei regulating the autonomic nervous system.
Purpose of the Study:
- To investigate the role of nesf/NUCB2 in blood pressure and ingestive behavior regulation.
- To utilize nesf/NUCB2-transgenic (Tg) mice to study these effects.
Main Methods:
- Measurement of blood pressure and heart rate in conscious and anesthetized Tg and non-Tg mice.
- Assessment of 24-hour water intake and urine volume using metabolic cages.
- Analysis of kidney weight and mRNA expression of epithelial sodium channel (ENaC)-α and ENaC-γ in the hypothalamus and kidney via real-time PCR.
Main Results:
- Tg mice exhibited significantly higher systolic, diastolic, and mean blood pressure, but not pulse rate, when conscious.
- Anesthesia abolished the elevated blood pressure in Tg mice.
- Tg mice showed increased water intake and urine volume, with lower urine sodium concentration but unchanged serum sodium and urine sodium excretion.
- Kidney weight was increased in Tg mice, with decreased hypothalamic ENaC-γ mRNA expression.
Conclusions:
- Nesf/NUCB2 plays a role in the central regulation of blood pressure.
- The findings suggest a brain-mediated mechanism involving nesf/NUCB2 in blood pressure control.
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