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Neuropeptide Y (NPY), neurotensin, arginine vasopressin (AVP), angiotensin II (ANG II), atrial natriuretic peptide (ANP) and calcitonin gene-related peptide (CGRP) have been suggested as putative neurotransmitters in the nucleus tractus solitarii (NTS) where baro- and chemoreceptor afferents terminate. To investigate modulation of the aortic baroreceptor reflex by neuropeptides, we microinjected these neuropeptides into the medial area of the rat NTS and examined their effects on the depressor and bradycardic responses to electrical stimulation of the aortic nerve which contains mainly baroreceptor afferent fibers in rats. Male Wistar rats were anesthetized with urethane, paralyzed and artificially ventilated. NPY (3 ng) and neurotensin (0.3 ng) injected into the NTS caused a decrease in blood pressure and/or heart rate, and facilitated the depressor and bradycardic responses to aortic nerve stimulation. AVP (3 ng) produced an increase in blood pressure and heart rate, and inhibited the responses to aortic nerve stimulation, whereas d(CH2)5Tyr(Me)AVP(100 ng), a V1 vasopressin receptor antagonist, did not affect the basal cardiovascular parameters and the baroreflex responses. ANG II (0.3 and 3 ng) caused a decrease in blood pressure and heart rate whereas at 0.3 ng it did not affect the baroreflex responses. ANP (3 ng) and CGRP (3 ng) did not affect the basal blood pressure and heart rate, and the responses to aortic nerve stimulation. These findings indicate that NPY, neurotensin and AVP microinjected into the rats NTS can modify the aortic baroreceptor reflex. Some of these neuropeptides may play a role in modulation of the aortic baroreceptor reflex within the NTS.
Neuropeptide Y (NPY), neurotensin, arginine vasopressin (AVP), angiotensin II (ANG II), atrial natriuretic peptide (ANP) and calcitonin gene-related peptide (CGRP) have been suggested as putative neurotransmitters in the nucleus tractus solitarii (NTS) where baro- and chemoreceptor afferents terminate. To investigate modulation of the aortic baroreceptor reflex by neuropeptides, we microinjected these neuropeptides into the medial area of the rat NTS and examined their effects on the depressor and bradycardic responses to electrical stimulation of the aortic nerve which contains mainly baroreceptor afferent fibers in rats. Male Wistar rats were anesthetized with urethane, paralyzed and artificially ventilated. NPY (3 ng) and neurotensin (0.3 ng) injected into the NTS caused a decrease in blood pressure and/or heart rate, and facilitated the depressor and bradycardic responses to aortic nerve stimulation. AVP (3 ng) produced an increase in blood pressure and heart rate, and inhibited the responses to aortic nerve stimulation, whereas d(CH2)5Tyr(Me)AVP(100 ng), a V1 vasopressin receptor antagonist, did not affect the basal cardiovascular parameters and the baroreflex responses. ANG II (0.3 and 3 ng) caused a decrease in blood pressure and heart rate whereas at 0.3 ng it did not affect the baroreflex responses. ANP (3 ng) and CGRP (3 ng) did not affect the basal blood pressure and heart rate, and the responses to aortic nerve stimulation. These findings indicate that NPY, neurotensin and AVP microinjected into the rats NTS can modify the aortic baroreceptor reflex. Some of these neuropeptides may play a role in modulation of the aortic baroreceptor reflex within the NTS.
The caudal ventrolateral medulla (CVLM) contains vasodepressor neurons which, when activated, decrease vasomotor tone. To investigate whether excitatory amino acid receptors in the CVLM of the rat are involved in mediation of the aortic baroreceptor reflex, we microinjected amino acid antagonists unilaterally into the CVLM and examined their effects on the depressor response to electrical stimulation of the aortic nerve which contains mainly baroreceptor afferent fibers in rats. Male Wistar rats were anaesthetized with urethane, paralyzed and artificially ventilated. To block reflex vagal effects, methylatropine (1 mg/kg) was given intravenously. Kynurenate (227 ng), an excitatory amino acid antagonist, injected ipsilaterally but not contralaterally into the CVLM markedly inhibited the depressor response to aortic nerve stimulation, while both injections produced a similar small increase in basal blood pressure. Muscimol (1 ng), a GABA receptor agonist, injected ipsilaterally into the CVLM partly inhibited the baroreflex response, while it produced a moderate increase in basal blood pressure. 2-Amino-5-phosphonovalerate (APV) (10 ng), a N-methyl-D-aspartate (NMDA) receptor antagonist, and MK-801 (30 ng), a NMDA receptor channel blocker, partly inhibited the baroreflex response. MK-801 (30 ng) injected into the CVLM reduced the depressor response to the NMDA receptor agonist NMDA (0.3 ng) but not to the quisqualate receptor agonist quisqualate (0.1 ng) and the kainate receptor agonist kainate (0.1 ng), while kynurenate (227 ng) inhibited the depressor response to all three excitatory amino acid receptor agonists. These findings provide further evidence for the presence of excitatory amino acid receptors involved in mediating the aortic baroreceptor reflex in the rat CVLM.(ABSTRACT TRUNCATED AT 250 WORDS)
Excitatory amino acid receptors and L-glutamate in the nucleus tractus solitarii (NTS) may be involved in the regulation of baroreceptor reflexes. To evaluate this hypothesis, we microinjected amino acid antagonists unilaterally into the rat NTS, and examined their effects on cardiovascular responses to electrical stimulation of the aortic nerve and on depressor responses to excitatory amino acid agonists microinjected into the NTS. Male Wistar rats were anesthesized with urethane, paralyzed, and artificially ventilated. Kynurenate (227 ng), an excitatory amino acid antagonist, injected ipsilaterally but not contralaterally into the NTS, markedly inhibited the depressor response to aortic nerve stimulation. L-Glutamate diethylester (GDEE, 3 micrograms), another excitatory amino acid antagonist, injected ipsilaterally into the NTS, also markedly inhibited both reflex depressor and bradycardic responses. MK-801 (30 ng), an N-methyl-D-aspartate (NMDA) receptor channel blocker, slightly inhibited the baroreflex responses, while Joro spider toxin JSTX-3 (17 ng), a glutamate receptor antagonist, did not affect them. Kynurenate (227 ng) and GDEE (3 micrograms) markedly inhibited the depressor response to the NMDA receptor agonist NMDA (0.3 ng), the quisqualate receptor agonist quisqualate (0.1 ng), the kainate receptor agonist kainate (0.1 ng), and L-glutamate (10 ng), microinjected into the NTS, while MK-801 (30 ng) reduced only the depressor response to NMDA (0.3 ng), and JSTX-3 (17 ng) reduced only the depressor response to kainate (0.1 ng). These findings provide evidence for the presence of excitatory amino acid receptors involved in mediating the aortic baroreceptor reflex in the rat NTS.(ABSTRACT TRUNCATED AT 250 WORDS)
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