Role of carbon monoxide in l-glutamate-induced cardiovascular responses in nucleus tractus solitarius of conscious rats

Abstract

Heme oxygenase degrades heme to form carbon monoxide. It has been reported that heme oxygenase-derived carbon monoxide may interact with l-glutamate ( l-Glu) receptors in the nucleus tractus solitarius (NTS). Integrative studies suggest that heme oxygenase inhibitors raise blood pressure, in part, by inhibiting carbon monoxide formation in the NTS. The currents studies were designed to determine if heme oxygenase inhibitors affect the cardiovascular actions of l-Glu in the NTS. Accordingly, MAP and HR responses to unilateral microinjections of l-Glu (5 nmol/100 nl) into the NTS were measured before and after ipsilateral microinjections of zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG, 4.5 nmol/100 nl) or chromium mesoporphyrin (CrMP, 1.5 nmol/100 nl) in awake rats chronically instrumented with NTS guide cannulaes and arterial catheters. With respect to non-treatment (+36±5 mmHg, −107 bpm, n=10), ZnDPBG pre-treatment attenuated the pressor and bradycardic responses to l-Glu (+7±3 mmHg, −10±6 bpm, P<0.05). CrMP similarly attenuated cardiovascular responses to l-Glu (+47±3 mmHg, −68±8 bpm vs. +20±5 mmHg, −40±9 bpm; before vs. after, n=10, P<0.05). Matched series yielded no vehicle- or time-related effects. Our findings suggest that a heme oxygenase product, such as carbon monoxide, may affect NTS glutamatergic neurotransmission to participate in cardiovascular control.