Role of carbon monoxide in L-glutamate-induced cardiovascular responses innucleus tractus solitarius of conscious rats

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 studi es 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 cardiovascul ar actions of L-Glu in the NTS. Accordingly, MAP and HR responses to unilat eral microinjections of L-Glu (5 nmol/100 nl) into the NTS were measured be fore 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 an d arterial catheters. With respect to non-treatment (+ 36 +/- 5 mmHg, - 107 bpm, n = 10), ZnDPBG pre-treatment attenuated the presser and bradycardic responses to L-Glu (+7 +/- 3 mmHg, - 10 +/- 6 bpm, P < 0.05). CrMP similarl y 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 contro l. (C) 1999 Elsevier Science B.V. All rights reserved.