Effect of the non-N-Methyl-D-aspartate receptor of the glutamatergic system of the pedunculopontine tegmental nucleus on cardiovascular responses in normotensive and hydralazine-induced hypotensive rats

Glutamate is an important excitatory neurotransmitter in the pedunculopontine tegmental (PPT) nucleus. The cardiovascular effect of glutamate and its non‑N‑methyl‑D‑aspartate (NMDA) receptor in the PPT is unknown; therefore, we evaluated glutamate and its non‑NMDA receptor on cardiovascular parameters in normotensive and hypotensive induced by hydralazine (HLZ) in rat.

After anesthesia, the femoral artery was cannulated for recording of cardiovascular parameters. Microinjection of drugs was done stereotaxically. L‑Glutamate (L‑Glu) and 6‑cyano‑7‑nitroquinoxaline‑2,3‑dione (CNQX) (an antagonist of nonNMDA receptor) were microinjected into the PPT in normotensive and HLZ hypotensive rats. Changes (∆) of mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were obtained and compared with the control group.

In normotensive rats, L‑Glu significantly increased SBP and MAP (P < 0.001) and decreased HR (P < 0.01), whereas CNQX alone did not significantly effect. Coinjection L‑Glu + CNQX significantly attenuates the cardiovascular effect of L‑Glu (P < 0.05 to P < 0.01). In hypotension induced by HLZ, SBP and MAP significantly decrease but HR did not change. In HLZ groups, L‑Glu significantly improves (P < 0.05) and CNQX deteriorated hypotension induced by HLZ (P < 0.05). Coinjection of L‑Glu + CNQX also attenuates the effect of L‑Glu on ∆ MAP and ∆ SBP. In hypotension, ∆HR induced by L‑Glu was significantly higher than CNQX (P < 0.01). In L‑Glu + CNQX group, ∆HR also was lower than L‑Glu (P < 0.05).

Our findings revealed that glutamatergic system of the PPT in both normotensive and hypotension induced by HLZ plays a pressor with bradycardic responses that partly mediated by non‑NMDA receptor.