Pressor responses of angiotensin II microinjected into the dorsomedial medulla of the dog

Averill, David B.; Diz, Debra I.; Barnes, Karen L.; Ferrario, Carlos M.

doi:10.1016/0006-8993(87)90009-6

Cited by 33 publications

(14 citation statements)

References 17 publications

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“…Previous studies indicate that acute microinjection of this peptide into the medial portion of the NTS produces either decreases or increases in BP (1,7,9,38). This controversy has been explained in several ways, for example, differences in the volume injected, dose, and region of the ANG II injection.…”

Section: Discussionmentioning

confidence: 92%

“…The central nervous system (CNS)-mediated cardiovascular actions of angiotensin II (ANG II) include stimulation of sympathetic nervous system (SNS) outflow, vasopressin release, and dampening of baroreflexes, via stimulation of angiotensin type 1 receptors (AT 1 R) in the nucleus tractus solitarii (NTS), a brain area that makes an important contribution to baroreflex integration and BP regulation (21,30). Acute microinjection of ANG II into the medial portion of the NTS produces decreases or increases in BP depending on the volume injected, dose, and region of the ANG II injection (1,7,9,38). The cardiovascular actions of ANG II are mediated not only by acute modulation of neuronal transmission and neuronal activity but also via changes in gene expression that influence long-term BP regulation.…”

mentioning

confidence: 99%

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Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats

Yao¹,

Sumners²,

O’Rourke³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Increasing evidence indicates that both the angiotensin II (ANG II) and gamma-aminobutyric acid (GABA) systems play a very important role in the regulation of blood pressure (BP). However, there is little information concerning the interactions between these two systems in the nucleus tractus solitarii (NTS). In the present study, we examined the effects of ANG II on GABAA and GABAB receptor (GAR and GBR) expression in the NTS of Sprague-Dawley rats. The direct effect of ANG II on GBR expression was determined in neurons cultured from NTS. Treatment of neuronal cultures with ANG II (100 nM, 5 h) induced a twofold increase in GBR1 expression, as detected with real-time RT-PCR and Western blots, but had no effect on GBR2 or GAR expression. In electrophysiological experiments, perfusion of neuronal cultures with the GBR agonist baclofen decreased neuronal firing rate by 39% and 63% in neurons treated with either PBS (control) or ANG II, respectively, indicating that chronic ANG II treatment significantly enhanced the neuronal response to GBR activation. In contrast, ANG II had no significant effect on the inhibitory action of the GAR agonist muscimol. In whole animal studies, intracerebroventricular infusion of ANG II induced a sustained increase in mean BP and an elevation of GBR1 mRNA and protein levels in the NTS. These results indicate that ANG II stimulates GBR expression in NTS neurons, and this could contribute to the central nervous system actions of ANG II that result in dampening of baroreflexes and elevated BP in the central actions of ANG II.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats

Yao¹,

Sumners²,

O’Rourke³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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show abstract

“…Electrophysiological and pharmacological studies suggest the participation of the 12 in multiple physiological responses subserving respiration, dipsogenesis (Yang et al 1997), and cardiovascular responses to hypothalamic defense area stimulation (St. Lambert et al 1996) or to direct angiotensin II injection (Averill et al 1987). The presence of B 2 receptors at these nuclei, in humans, supports the participation of BK in the mediation of viscerosensory processes, mainly in cardiovascular control.…”

Section: Vagal Solitary Complexmentioning

confidence: 94%

Autoradiographic detection of kinin receptors in the human medulla of control, hypertensive, and diabetic donors

Buck

Ongali²,

Thibault³

et al. 2002

Can. J. Physiol. Pharmacol.

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Kinins have been elected to the status of central neuromediators. Their effects are mediated through the activation of two G-protein-coupled receptors, denoted B, and B2. Functional and binding studies suggested that B1 and B2 receptors are upregulated in the medulla and spinal cord of hypertensive and diabetic rats. The aim of this study was to localize and quantify kinin receptors in post-mortem human medulla obtained from normotensive, hypertensive, and diabetic subjects, using in vitro receptor autoradiography with the radioligands [125I]HPP-HOE140 (B2 receptor) and [125I]HPP[des-Arg10]-HOE140 (B1 receptor). Data showed specific binding sites for B2 receptor (0.4-1.5 fmol/mg tissue) in 11 medullary nuclei from 4 control specimens (paratrigeminal > ambiguus > cuneate, gelatinous layer of the caudal spinal trigeminal nucleus > caudal and interpolar spinal trigeminal, external cuneate, solitary tract > hypoglossal > gracile > inferior olivary nuclei). Increased density of B2 receptor binding sites was observed in seven medullary nuclei of four hypertensive specimens (paratrigeminal > external cuneate > interpolar and caudal spinal trigeminal, gracile, inferior olivary > hypoglossal nuclei). B2 receptor binding sites were seemingly increased in the same medullary nuclei of two diabetic specimens. Specific binding sites for B1 receptor (1.05 and 1.36 fmol/mg tissue) were seen only in the inferior olivary nucleus in two out of the ten studied specimens. The present results support a putative role for kinins in the regulation of autonomic, nociceptive, and motor functions at the level of the human medulla. Evidence is also provided that B2 receptors are upregulated in medullary cardiovascular centers of subjects afflicted of cardiovascular diseases.

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“…3 7 Recently, we have shown that microinjection of Ang II into the AP or medial NTS of the dog elicits increases in blood pressure and heart rate. 8 In addition, the discovery of a high density of Ang II binding sites in the canine DMM that depend on the vagal innervation of these structures reinforces the cardiovascular importance of Ang II in this region. 9 The present experiments have begun to address the question of whether angiotensin peptides regulate transmission in neuronal pathways related to cardiovascular function by determining the capacity of Ang II to alter neuronal activity in the canine DMM.…”

mentioning

confidence: 89%

Neuronal responses to angiotensin II in the in vitro slice from the canine medulla.

1988

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SUMMARY The present studies utilized the in vitro slice preparation of the canine dorsomedial medulla, which we have recently developed, to obtain direct evidence for the effects of angiotensin II (Ang II) on the activity of single neurons in this region. Horizontally oriented slices (300 fxm) containing the area postrema, nucleus tractus solitarii (NTS), and dorsal motor nucleus of the vagus were perifused with oxygenated artificial cerebrospinal fluid. The effects of microdrop application of Ang II and its antagonist [Sar',Thr 8 ]Ang II on spontaneous firing rate were determined in 27 extracellularly recorded neurons. Ang II substantially increased the firing rate of 13 neurons located in the medial NTS, but it did not alter the spontaneous activity of the remaining 14 neurons. In most cases Ang II elicited a slowly developing, prolonged excitatory response. The effects of both Ang II and [Sar',Thr*]Ang II were tested in 13 neurons. [Sar^Thr'JAng II produced a short latency, brief excitation in three neurons, marked inhibition of spontaneous firing in two cells, and no effect on the other eight neurons. Administration of [Sar^Thr^Ang II blocked the excitatory effects of subsequent administration of Ang II in three neurons. To our knowledge, these observations provide the first evidence for direct actions of both Ang II and O UR previous investigations of the canine dorsomedial medulla (DMM) have provided substantial evidence that the area postrema (AP) and nucleus tractus solitarii (NTS) exert reciprocal influences on both tonic and reflex control of blood pressure. Initial studies revealed that small amounts of angiotensin II (Ang II) given into the vertebral arteries produce a pressor response mediated by the AP.1 Subsequent investigations documented that the AP contains a neural pressor pathway that counterbalances the vasodepressor actions of the baroreceptor relay in the adjacent NTS.2 "* A role for these structures in the tonic regulation of the cardiovascular system has been underscored by the observations that lesions of either the AP or the NTS result in lasting alterations of cardiovascular function.3 7 Recently, we have shown that

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Pressor responses of angiotensin II microinjected into the dorsomedial medulla of the dog

Cited by 33 publications

References 17 publications

Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats

Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats

Autoradiographic detection of kinin receptors in the human medulla of control, hypertensive, and diabetic donors

Neuronal responses to angiotensin II in the in vitro slice from the canine medulla.

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Pressor responses of angiotensin II microinjected into the dorsomedial medulla of the dog

Cited by 33 publications

References 17 publications

Angiotensin II increases GABAB receptor expression in nucleus tractus solitarii of rats

Angiotensin II increases GABAB receptor expression in nucleus tractus solitarii of rats

Autoradiographic detection of kinin receptors in the human medulla of control, hypertensive, and diabetic donors

Neuronal responses to angiotensin II in the in vitro slice from the canine medulla.

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Product

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Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats

Angiotensin II increases GABA_B receptor expression in nucleus tractus solitarii of rats