Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Wang, H. et al.

Brain sodium channels and central sodium-induced increases in brain ouabain-like compound and blood pressure.

OBJECTIVE: To assess the role of benzamil-sensitive sodium channels in the increases in brain ouabain-like compounds (OLC) and in blood pressure by cerebrospinal fluid (CSF) Na+. METHODS: Artificial CSF (aCSF) or Na+-rich (0.8 mol/l Na+) aCSF, either alone or combined with benzamil (at 1.2 and 4.0 microg/kg per h), were infused intracerebroventricularly (i.c.v.) at 5 microl/h to Wistar rats for 14 days and the effects on the brain and peripheral OLC and blood pressure were studied. OLC content was measured by enzyme-linked immunosorbent assay. RESULTS: In Wistar rats infused i.c.v. with aCSF, benzamil did not affect blood pressure or brain and peripheral OLC concentrations. I.c.v. infusion of Na+-rich aCSF increased systolic blood pressure (140 +/- 4 mmHg compared with 119 +/- 3 mmHg; P < 0.05). Benzamil fully blocked this increase. Na+-rich aCSF increased hypothalamic (23 +/- 3 ng/g tissue compared with 10 +/- 1 ng/g tissue; P < 0.05) and pituitary (233 +/- 35 ng/g tissue compared with 62 +/- 7 ng/g tissue; P < 0.05) contents of OLC. In contrast, Na+-rich aCSF decreased OLC in the adrenal gland (7 +/- 1 ng/g tissue compared with 21 +/- 3 ng/g tissue; P < 0.05) and plasma (0.5 +/- 0.04 ng/ml compared with 0.7 +/- 0.08 ng/ml; P < 0.05). Benzamil inhibited these responses of OLC to CSF sodium in a dose-related manner. CONCLUSIONS: These findings suggest that benzamil-sensitive brain sodium channels mediate the increase in brain OLC and the subsequent hypertension induced by increased CSF Na+.[1]

References

Brain sodium channels and central sodium-induced increases in brain ouabain-like compound and blood pressure. Wang, H., Leenen, F.H. J. Hypertens. (2003) [Pubmed]

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