Abstract
A neural mechanism responsible for sympathetic activation in HT rats was investigated. We hypothesized that reduced SK current in PVN‐RVLM neurons could contribute to increased excitability and sympathoexcitation in HT rats. In voltage‐clamp recordings, the amplitude of SK current was significantly reduced in neurons from HT rats. In current‐clamp recordings, the frequency of current injection‐evoked spikes was greater in neurons from HT rats compared to normotensive (NT) controls. The SK channel blocker apamin caused a greater increase in spikes in NT controls compared to HT group. The amplitude of a medium after‐hyperpolarization potential (mAHP) was significantly reduced in the HT group. An after‐depolarization potential (ADP) was also observed in the HT group, but not in NT controls, though apamin did reveal an ADP in NT controls while failing to alter the ADP already present in the HT group. This suggests that diminished SK current likely underlies the smaller mAHP and the uncovered ADP in the HT group. Microinjection of apamin into the PVN of anesthetized rat induced a greater increase in renal SNA and MAP in NT compared to HT rats. We conclude that increased excitability of PVN‐RVLM neurons may contribute to sympathoexcitation and maintenance of AngII‐salt hypertension and reduced SK current in these neurons may constitute an underlying neural mechanism. Support: AHA0865107F (CQH) & HL076312 (GMT).
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