| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Sympathoexcitation plays a crucial role in hypertension with chronic kidney disease (CKD). Paraventricular nucleus of the hypothalamus (PVN) in the brain controls sympathetic outflow through GABA-ergic input. Renal denervation (RDN) exerts an antihypertensive effect in hypertension with CKD; however the mechanisms are not known. We sought to elucidate whether RDN modulates sympathetic outflow through GABA-ergic input into the PVN in hypertensive mice with CKD.
In 5/6-nephrectomized ICR-mice (Nx), systolic blood pressure (SBP) was increased with sympathoexcitation. We performed RDN(Nx-RDN) or sham(Nx-Sham). SBP and sympathetic nerve activity (SNA) were decreased in Nx-RDN. GABA-A receptor antagonist injection into the PVN increased arterial pressure and lumbar SNA(LSNA) in Nx. The pressor and LSNA responses were attenuated in Nx-Sham, but were enhanced in Nx-RDN.
Augmented GABA-ergic input into the PVN induced by RDN is involved in antihypertensive effect in hypertensive mice with CKD.
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