Insulin microinjection into the nucleus tractus solitarii of the rat attenuates the baroreceptor reflex.

The presence of insulin and insulin binding sites in the central nervous system and the demonstration that central insulin has an effect on cardiovascular function has led to the hypothesis that insulin may play a role in mediating the baroreceptor reflex. To investigate this possibility, insulin was microinjected into depressor sites in the nucleus tractus solitarius (NTS), the first central synapse of the baroreceptor reflex, of urethane anesthetized rats. Microinjection of insulin into the NTS (110 nL of 1, 10 and 100 IU/mL) did not change mean arterial pressure (MAP) or heart rate (HR). However, insulin microinjection attenuated phenylephrine-elicited reflex bradycardia and depressor responses elicited by glutamate (GLU). The attenuation of GLU-elicited depressor responses was time-dependent for MAP changes and time and concentration-dependent for HR changes (p < 0.05). Insulin-like growth factor-1 microinjection into the NTS also attenuated GLU-elicited decreases in MAP (p < 0.05) but not HR. The effect of insulin on GLU-elicited responses was inhibited after peripheral adrenergic blockade by nadolol (1.0 mg/kg i.v.) but not after cholinergic blockade by methyl-atropine (2.0 mg/kg i.v.). These results demonstrate that insulin inhibits baroreceptor reflex responses in the NTS likely through an influence on the effects of excitatory amino acid neurotransmitters on the activity of NTS neurons involved in sympathetic control of the cardiovascular system.