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Angiotensin II excites vasomotor neurons but not respiratory neurons in the rostral and caudal ventrolateral medulla.

We examined the vasomotor and respiratory effects of angiotensin II microinjection into the rabbit ventrolateral medulla (VLM). Angiotensin II in the rostral and caudal VLM increased and decreased arterial pressure, respectively, but had no effect on phrenic nerve activity. In contrast, L-glutamate injections in the same areas altered both arterial pressure and phrenic nerve activity. The results suggest that angiotensin II may activate specifically vasomotor neurons but not respiratory neurons in the VLM.

Angiotensin II↗

Differential contribution of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors in the intermediolateral cell column of the thoracic spinal cord to sympathetic vasomotor tone during experimental endotoxemia in the rat.

Although the rostral ventrolateral medulla maintains neurogenic vasomotor tone via glutamatergic excitation to sympathetic preganglionic neurons located at the intermediolateral cell column (IML) of thoracic spinal cord, the relative contribution of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on IML neurons at rest or during endotoxemia remain unknown. The present study addressed this issue using a combination of physiological, pharmacological, and double-immunofluorescence approaches. Adult male Sprague-Dawley rats maintained under propofol anesthesia were used. Intrathecal administration of equimolar concentrations (75, 150, or 300 nmol) of an NMDA antagonist, dizocilpine (MK801), or a non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, into T10 to T12 spinal cord elicited a reduction in resting vasomotor tone that was comparable in time course and in magnitude. Although both glutamate receptor antagonists exacerbated mortality and potentiated the elicited hypotension, bradycardia, or reduction in vasomotor tone during experimental endotoxemia induced by intravenous administration of Escherichia coli lipopolysaccharide (30 mg kg-1; results comparable to 6-cyano-7-nitroquinoxaline-2,3-dione at 150 nmol) were obtained only when MK801 was given at 300 nmol. Confocal microscopy further showed that augmented immunoreactivity of NR1 subunit on IML neurons coincided with the phase of endotoxemia when vasomotor tone was augmented; GluR1 immunoreactivity remained stable throughout experimental endotoxemia. These findings suggest that NMDA and non-NMDA receptors on IML neurons contribute to the generation of resting sympathetic vasomotor tone. However, up-regulation of NMDA receptors on IML neurons plays a crucial role in the maintenance of vasomotor tone during endotoxemia.

Animals↗