1982
DOI: 10.1016/0024-3205(82)90576-8
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Potentiation of the carotid artery occlusion reflex by a cholinergic system in the posterior hypothalamic nucleus

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Cited by 19 publications
(4 citation statements)
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“…The inhibitory effect of atropine upon the cardiac parasympathetic nerves is thought to have been functionally maintained throughout the experiment, since a bolus injection of atropine administered at the end of the experiment did not increase the HR. Though a baroreflex HR increase can be achieved not only by sympathetic nerve activation but also by cardiac parasympathetic nerve inhibition (Brezenoff et al 1982;Ferrari et al 1991), our results indicated that the CAO-evoked HR increase was controlled by the sympathetic nervous system under our conditions. Even if the HR did not change after SCT it would not mean that the cardiac sympathetic nerve was unaffected by the transection, because the parasympathetic effects could compensate for the HR changes.…”
Section: Discussionmentioning
confidence: 53%
“…The inhibitory effect of atropine upon the cardiac parasympathetic nerves is thought to have been functionally maintained throughout the experiment, since a bolus injection of atropine administered at the end of the experiment did not increase the HR. Though a baroreflex HR increase can be achieved not only by sympathetic nerve activation but also by cardiac parasympathetic nerve inhibition (Brezenoff et al 1982;Ferrari et al 1991), our results indicated that the CAO-evoked HR increase was controlled by the sympathetic nervous system under our conditions. Even if the HR did not change after SCT it would not mean that the cardiac sympathetic nerve was unaffected by the transection, because the parasympathetic effects could compensate for the HR changes.…”
Section: Discussionmentioning
confidence: 53%
“…Earlier studies showed that the pressor effect of bilateral carotid occlusion was greater after central or systemic administration of physostigmine. 8,17 Caputi et al demonstrated an upward shift in baroreflex HR responses without changes in range or gain following intracerebroventricular injection of physostigmine. 16 A limitation of the present study was that pretreatment with mATR to block peripheral mAChR precluded analysis of vagally mediated HR responses.…”
Section: Padley Et Al Cholinergic Inputs To Rvlm In Central Commandmentioning
confidence: 99%
“…[7][8][9][10][11][12][13][14][15][16][17][18] Systemic or central administration of acetylcholinesterase inhibitors or muscarinic agonists increases blood pressure, 7-11 lowers body temperature, 12 and alters respiration. 13,14 Pressor responses can be evoked via activation of muscarinic receptors (mAChR) within several cardiovascular nuclei, including the posterior hypothalamus, 7 nucleus of the solitary tract, 15 and rostral ventrolateral medulla (RVLM).…”
Section: ;100:284-291)mentioning
confidence: 99%
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