Modulation of the arterial baroreflex by the hypothalamic paraventricular nucleus.

Previous studies have demonstrated that nonspecific activation or inhibition of the paraventricular nucleus (PVN) alters arterial baroreflex (BR) function. However, the action of specific neurotransmitters is unclear. PVN pre‐autonomic neurons are tonically inhibited by γ‐amino butyric acid (GABA) input. Moreover, disinhibition of the PVN by microinjection of the GABA A receptor antagonist, bicuculline (BIC), increases arterial pressure (AP), heart rate (HR), and sympathetic activity. Therefore, in urethane‐anesthetized female rats (n=5), we tested the hypothesis that PVN GABAergic tone inhibits BR function, by determining if BR gain increases ∼5 min following unilateral PVN microinjection of BIC (60 pmol). BR function was quantified by a 4 parameter sigmoidal fit of HR responses to slow ramp changes in AP, induced by first infusing nitroprusside to quickly lower AP to ∼50 mmHg, followed by infusion of phenylephrine to raise AP to ∼150 mmHg over 3–4 min. PVN BIC increased (P<0.05) AP (by 12±3 mmHg from 112±3 mmHg) and HR (by 17±4 bpm from 363±17 bpm). BR gain increased (P<0.01) from 1.9±0.4 to 6.0±2.2 bpm/mmHg. In addition, PVN BIC increased (P<0.05) maximum baroreflex HR from 386±8 to 440±20 bpm; however, no other sigmoidal parameters were significantly altered. In summary, PVN GABAergic input tonically inhibits arterial BR function by suppressing BR gain and the maximal level of HR achieved at low BP.