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1 Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA
2 School of Veterinary Medicine, Purdue University, West Lafayette, Indiana, USA
3 Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon, USA
* To whom correspondence should be addressed. E-mail: barnesk{at}ccf.org.
Femtomole (fmol) doses of angiotensin (Ang) II microinjected into nucleus tractus solitarii (nTS) decrease blood pressure and heart rate, mimicking activation of the baroreflex, whereas higher doses depress this reflex. Ang II might generate cardioinhibitory responses by augmenting cardiovascular afferent synaptic transmission onto nTS neurons. Intracellular recordings from 99 dorsal medial nTS region neurons in rat medulla horizontal slices investigated whether Ang II modulated short-latency excitatory postsynaptic potentials (EPSPs) evoked by solitary tract (TS) stimulation. Ang II (200 fmol) increased TS-evoked EPSP amplitudes 20-200% with minimal membrane depolarization in 12 neurons excited by Ang II and glutamate, but not substance P (Group A). Blockade of non-N-methyl-D-aspartate (non-NMDA) receptors eliminated TS-evoked EPSPs and responses to Ang II. Ang II did not alter TS-evoked EPSPs in 14 other neurons depolarized substantially by both Ang II and substance P (Group B). Ang II appeared to selectively augment presynaptic sensory synaptic transmission in one class of nTS neurons, but had only postsynaptic effects on another group of cells. Thus Ang II is likely to modulate cardiovascular function by more than one nTS neuronal pathway.
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