Stimulation of the Prorenin Receptor in the Paraventricular Nucleus Increases Sympathetic Outflow in Anesthetized Rat

TL;DRAbstract

Previous studies indicate that activation of brain prorenin receptors (PRR) contributes to hypertension. However, the detailed mechanism underlying the role of brain PRR on blood pressure control is not well understood. Here we investigated the hypothesis that stimulation of PRR in the hypothalamic paraventricular nucleus (PVN) results in an increase in sympathetic nerve activity (SNA) and therefore contributes to neurogenic hypertension. In anaesthetized adult Sprague Dawley (SD) rats, bilateral PVN microinjection of prorenin (2 pmol/side) increased splanchnic SNA (SSNA) (71±15%, n=7) and renal SNA (RSNA) (21±10%, n=7). Pre‐injection of the prorenin handle region peptide, a PRR binding blocker (PRRB), into the PVN, significantly attenuated the elevation in the SSNA (32±5%; p<0.05 vs. vehicle control; n=6) but did not block the increase in RSNA (3±11%; p=0.24 vs vehicle control; n=7) evoked by prorenin injection. We further investigated the effect of PRR activation on downstream gen

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