Role of Acetylcholine, Corticoids and Opioids in the Rostral Ventrolateral Medulla in Stress-Induced Hypertensive Rats

Li, P.; Zhu, Dawei; Kao, Kung‐Chun; Qi, Lin; Sun, Shuxin

doi:10.1159/000109432

Cited by 12 publications

(7 citation statements)

References 18 publications

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“…38 The -and ␦-, but not the -, opioid receptors of the rVLM, are activated to induce the depressor effect under resting conditions. 39 Thus previous studies of the central neural structures activated by MNS have documented the presence of an important inhibitory effect on sympathetically mediated vasoconstriction. Although these studies did not investigate the response to stimulation of the median nerve during reflex activation of the sympathetic nervous system, it is possible that similar pathways and the endogenous opioid system are involved in the diminished pressor and double product reflex responses during gallbladder stimulation.…”

Section: Discussionmentioning

confidence: 95%

Reversal of Reflex-Induced Myocardial Ischemia by Median Nerve Stimulation

et al. 1998

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Background-Acupuncture is reported to reduce myocardial ischemia, arrhythmias, and hypertension. To investigate the physiological mechanisms underlying these observations, a model of reflex-induced, reversible myocardial ischemia was developed to test the effects of median nerve stimulation as a surrogate for electroacupuncture. Methods and Results-Chloralose-anesthetized cats were instrumented to measure arterial blood pressure, left ventricular pressure, left ventricular dP/dt, heart rate, left anterior descending (LAD) coronary blood velocity, and regional wall motion. The LAD artery either was partially occluded or a small diagonal branch was ligated. Subsequently, transient reflex activation of the cardiovascular system was evoked by application of bradykinin (typically 1 g/mL) to the gallbladder, which significantly increased myocardial oxygen demand (double product), left ventricular dP/dt, and coronary blood velocity and caused ischemia-induced regional dysfunction, evidenced by significant (PϽ.05) reduction in normalized wall thickening (10.7Ϯ4.2% versus Ϫ23.6Ϯ2.9%; control versus ischemia; nϭ7). However, when median nerves were stimulated with low frequency (5 Hz) to mimic electroacupuncture, bradykinin-induced change in normalized wall thickening was significantly improved (Ϫ23.6Ϯ2.9% versus 9.8Ϯ4.9%; ischemia versus median nerve stimulation, PϽ.05) and remained augmented Ն1 hour. Results were similar in partial and complete occlusion groups. Significant improvement in wall thickening was associated with unchanged increment of coronary blood velocity and significantly diminished increments of double product and diastolic blood pressure. Conclusions-These results suggest that stimulation of the median nerve to mimic electroacupuncture diminishes regional myocardial ischemia triggered by a sympathetically mediated increase in cardiac oxygen demand. The mechanism of this effect is related to reduction in cardiac oxygen demand, secondary to a diminished pressor response. These data provide the first documentation of the physiological mechanisms underlying the possible beneficial effect of electroacupuncture in the context of restricted coronary blood flow and augmented myocardial oxygen demand.

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Section: Discussionmentioning

confidence: 95%

Reversal of Reflex-Induced Myocardial Ischemia by Median Nerve Stimulation

et al. 1998

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“…Of the two major subtypes of cholinergic receptors, it is generally contended that the muscarinic receptors in the RVLM play a more prominent role than the nicotinic subtype in cardiovascular regulation. The RVLM is one of the brain substrates with the highest muscarinic receptor binding density (Kellar et al 1985; Arneric et al 1990), and acetylcholine acts preferentially through muscarinic receptors in this medullary region (Willette et al 1984; Li et al 1995) to elicit cardiovascular actions (Willette et al 1984; Kubo et al 1997) or neuronal responses (Huangfu et al 1997). Thus, it is conceivable that, while similarly acting on muscarinic M2R or M4R, the progressively accumulated acetylcholine in the RVLM because of Mev‐induced cholinesterase inhibition is responsible for our observed shift from an augmented power density of the low‐frequency component of SAP signals during the ‘pro‐life’ phase to a reduction of low‐frequency power during the ‘pro‐death’ phase.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional up‐regulation of nitric oxide synthase II by nuclear factor‐κB at rostral ventrolateral medulla in a rat mevinphos intoxication model of brain stem death

Chan

Tsai

et al. 2007

The Journal of Physiology

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As the origin of a 'life-and-death' signal that reflects central cardiovascular regulatory failure during brain stem death, the rostral ventrolateral medulla (RVLM) is a suitable neural substrate for mechanistic delineation of this vital phenomenon. Using a clinically relevant animal model that employed the organophosphate pesticide mevinphos (Mev) as the experimental insult, we evaluated the hypothesis that transcriptional up-regulation of nitric oxide synthase I or II (NOS I or II) gene expression by nuclear factor-κB (NF-κB) on activation of muscarinic receptors in the RVLM underlies brain stem death. In Sprague-Dawley rats maintained under propofol anaesthesia, co-microinjection of muscarinic M2R (methoctramine) or M4R (tropicamide), but not M1R (pirenzepine) or M3R (

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“…It is accepted that activation of sympathetic nervous system [23] and the RAS [24] play a role in the initiation of stress-induced hypertension. Li [25] found that increased activity of the cholinergic system in the rostral ventrolateral medulla (rVLM) was also involved in the development of stress-induced hypertension. Plasma catecholamine, corticosterone, angiotensin II, glucose, and lipids were found to be increased during stress.…”

Section: The Major Animal Models Of Hypertensionmentioning

confidence: 99%

Historic perspectives and recent advances in major animal models of Hypertension1

Sun

Zhang

2005

Acta Pharmacologica Sinica

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Hypertension and related cardiovascular diseases are the leading causes of death in many countries. The etiology of human essential hypertension is largely unknown. It is highly likely that hypertension is a complex and multifactorial disease resulting from the interaction of multiple genetic and environmental factors. Animal models of hypertension have been proved to be useful to study the pathogenesis of, and to find a new therapy for, hypertension. The aim of this article is to briefly review the most widely used rodent models of experimental hypertension, including history and recent advances. These models are classified as genetically-induced, environmentally-induced, pharmacologically-induced, and renalinduced hypertension according to the way of induction; the typical representatives of each of these major types of experimental hypertension are spontaneous hypertension, cold-induced hypertension, DOCA-salt-induced hypertension, and renal-induced hypertension, respectively. The processes of induction of hypertension, possible pathogenesis, characteristics, advantages, and limitations of these animal models are reviewed. In addition, the clinical implications of the above experimental models of hypertension are addressed.

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Role of Acetylcholine, Corticoids and Opioids in the Rostral Ventrolateral Medulla in Stress-Induced Hypertensive Rats

Cited by 12 publications

References 18 publications

Reversal of Reflex-Induced Myocardial Ischemia by Median Nerve Stimulation

Reversal of Reflex-Induced Myocardial Ischemia by Median Nerve Stimulation

Transcriptional up‐regulation of nitric oxide synthase II by nuclear factor‐κB at rostral ventrolateral medulla in a rat mevinphos intoxication model of brain stem death

Historic perspectives and recent advances in major animal models of Hypertension1

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