Antagonism of glutamatergic metabotropic receptors in the NTS of awake rats does not affect the gain of the baroreflex.

There is evidence suggesting that metabotropic receptors may play a role in the neurotransmission of the baroreflex in the nucleus tractus solitarius (NTS) of rats. In a recent study from our laboratory, we verified that microinjection of a metabotropic receptor agonist, trans-1-amino-1,3-cyclopentanediocarboxylic acid, into the NTS of awake and anesthetized rats produced baroreflex-like responses (hypotension and bradycardia). In the present study, we evaluated the possible role of L-glutamate metabotropic receptors of the NTS in the neuromodulation of the parasympathetic component of baroreflex activation in awake rats. Bilateral microinjection (50 nl) of a metabotropic receptor antagonist (alpha-methyl-4-carboxyphenylglycine, MCPG, 100 mM) into the rostral commissural NTS produced no change in the gain of the baroreflex bradycardia. In addition, microinjection of MCPG into the NTS produced no changes in baseline mean arterial pressure (MAP) or heart rate (HR), indicating that metabotropic receptors play no tonic role in the neurotransmission of the baroreflex. The dose of MCPG used to block the metabotropic receptors was effective in reducing the bradycardic and hypotensive responses to microinjection (50 nl) of trans-1-amino-1,3-cyclopentanediocarboxylic acid (5 mM) into the NTS. The data show that metabotropic glutamate receptors play no major role in the neuromodulation of the parasympathetic component of the baroreflex at the NTS level.