Mechanisms of autonomic control by the insular cortex in the rat

The insular cortex (IC) has been proposed to act as visceral sensory and autonomic cortex. The mechanism of control by the IC, however, is not clear. The nature of insular cortical function in hypertension is also unknown.;Middle cerebral artery occlusion (MCAO) in Wistar rats has been shown to cause cortical infarction, including the IC, resulting in increases in sympathetic nerve discharge (SND). MCAO in the urethane anesthetized spontaneously hypertensive rat (SHR) resulted in decreases in arterial pressure (AP) and SND.;To determine if the autonomic effects of MCAO in the SHR and Wistar rat are due to insular damage, a lesion of the IC was made, using an excitotoxic amino acid. Increases in SND were observed in Wistar rats and decreases in SHR's, similar to that seen following MCAO.;Systematic D,L homocysteate (DLH) injections into the IC of propofol-anesthetized Wistar rats resulted in a significant increase in AP and a significant decrease in HR and SND. DLH and lidocaine injections into the IC of conscious Wistar rats both resulted in a significant increase in AP. It was concluded that the IC of conscious Wistar rats has a tonic inhibitory output, while neural excitation is capable of eliciting pressor responses. The IC of SHR appeared to exert no tonic influence on AP.;Previous studies have shown sympathetic nerve responses to C stimulation are mediated by uncharacterized synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla (VLM). Glutamate antagonist injection into the ipsilateral VLM blocked IC and LHA sympathetic responses. A non-NMDA receptor antagonist also blocked IC and LHA sympathetic responses, while an NMDA antagonist was ineffective.;Glutamate antagonist injection into the ipsilateral LHA blocked IC sympathetic nerve responses. NMDA antagonist injection also inhibited IC sympathetic responses, while the non-NMDA antagonist had no effect.;These studies provide the most conclusive evidence that the IC is critical to the autonomic disruptions following stroke. The IC may also play a role in the pathogenesis of hypertension. The IC appears to have a tonic sympatho-inhibitory influence in normotensive animals, though a sympatho-excitatory response is possible. The IC sympathetic effects are mediated by an NMDA glutamatergic synapse in the LHA and a non-NMDA synapse in the VLM.