scholarly journals Enhancement in Tonically Active Glutamatergic Inputs to the Rostral Ventrolateral Medulla Contributes to Neuropathic Pain-Induced High Blood Pressure

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Wang ◽  
Zui Zou ◽  
Xing Tan ◽  
Ru-Wen Zhang ◽  
Chang-Zhen Ren ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Neuropathic Pain ◽  
Cardiovascular Diseases ◽  
High Blood Pressure ◽  
Glutamate Transporter ◽  
Rostral Ventrolateral Medulla ◽  
Infraorbital Nerve ◽  
Ventrolateral Medulla ◽  
Sympathetic Overactivity ◽  
High Level

Neuropathic pain increases the risk of cardiovascular diseases including hypertension with the characteristic of sympathetic overactivity. The enhanced tonically active glutamatergic input to the rostral ventrolateral medulla (RVLM) contributes to sympathetic overactivity and blood pressure (BP) in cardiovascular diseases. We hypothesize that neuropathic pain enhances tonically active glutamatergic inputs to the RVLM, which contributes to high level of BP and sympathetic outflow. Animal model with the trigeminal neuropathic pain was induced by the infraorbital nerve-chronic constriction injury (ION-CCI). A significant increase in BP and renal sympathetic nerve activity (RSNA) was found in rats with ION-CCI (BP, n=5, RSNA, n=7, p<0.05). The concentration of glutamate in the RVLM was significantly increased in the ION-CCI group (n=4, p<0.05). Blockade of glutamate receptors by injection of kynurenic acid into the RVLM significantly decreased BP and RSNA in the ION-CCI group (n=5, p<0.05). In two major sources (the paraventricular nucleus and periaqueductal gray) for glutamatergic inputs to the RVLM, the ION-CCI group (n=5, p<0.05) showed an increase in glutamate content and expression of glutaminase 2, vesicular glutamate transporter 2 proteins, and c-fos. Our results suggest that enhancement in tonically active glutamatergic inputs to the RVLM contributes to neuropathic pain-induced high blood pressure.

scholarly journals Participation of 5-HT and AT1Receptors within the Rostral Ventrolateral Medulla in the Maintenance of Hypertension in the Goldblatt 1 Kidney-1 Clip Model

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Cássia T. Bergamaschi ◽  
Nyam F. Silva ◽  
Jose G. Pires ◽  
Ruy R. Campos ◽  
Henrique A. Futuro Neto
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
High Blood Pressure ◽  
Wistar Rats ◽  
Kynurenic Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Receptor Blockade ◽  
Control Groups ◽  
Male Wistar Rats

The hypothesis that changes in neurotransmission within the rostral ventrolateral medulla (RVLM) are important to maintain the high blood pressure (BP) was tested in Goldblatt one kidney-one clip hypertension model (1K-1C). Male Wistar rats were anesthetized (urethane 1.2 g/kg, i.v.), and the effects of bilateral microinjections into the RVLM of the following drugs were measured in 1K-1C or control groups: glutamate (0.1 mol/L, 100 nL) and its antagonist kynurenic acid (0.02 mol/L, 100 nL), the angiotensin AT1receptor antagonist candesartan (0.01 mol/L, 100 nL), and the nonselective 5-HT receptor antagonist methiothepin (0.06 mol/L, 100 nL). Experiments in 1K-1C rats were performed 6 weeks after surgery. In anesthetized rats glutamate response was larger in hypertensive than in normotensive rats (H:Δ67±6.5; N:Δ43±3.54 mmHg). In contrast, kynurenic acid microinjection into the RVLM did not cause any change in BP in either group. The blockade of either AT1or 5-HT receptors within the RVLM decreased BP only in 1K-1C rats. A largest depressor response was caused by 5-HT receptor blockade. The data suggest that 5-HT and AT1receptors act tonically to drive RVLM in 1K-1C rats, and these actions within RVLM contribute to the pathogenesis of this model of hypertension.

scholarly journals A CASE STUDY ON ESSENTIAL HYPERTENSION MANAGING THROUGH AYURVEDA W.S.R. RAKTAGATA VYAN VAISHAMYA

2021 ◽  
Vol p5 (4) ◽  
pp. 2965-2968
Author(s):  
Ruhi Zahir ◽  
Iqbal Khan
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Risk Factor ◽  
Essential Hypertension ◽  
Cardiovascular Diseases ◽  
High Blood Pressure ◽  
Direct Reference ◽  
Major Risk Factor ◽  
End Stage

Essential hypertension is high blood pressure that doesn't have any known etiopathology. Most of sufferers (85%) are asymptomatic and as per available reports, in more than 95% cases of hypertension under lying cause is not found. It is estimated that 600 million people are affected worldwide. Hypertension is a major risk factor for the development of cardiovascular diseases (CVD). Its impact is greatest on stroke, MI and end stage is renal failure as it’s known as a Silent Killer. Hence there is no direct reference of hypertension in Ayurvedic classics by name as well as by its path physiological views. Many works have been carried out on hypertension to evaluate the perfect diagnosis and mode of treatment on the basis of Different nomenclatures also have been adopted by Ayurveda experts like Raktagata Vata, Raktagata Vyana Vaisamya, Uccha Rakta Chapa, Raktavrita Vata, Siragata Vata etc. Keywords: Essential hypertension, Raktagata Vyana Vaisamya, Uccha Rakta Chapa, Cardiovascular diseases, Silent Killer.

scholarly journals Overexpression of Central ACE2 (Angiotensin-Converting Enzyme 2) Attenuates the Pressor Response to Chronic Central Infusion of Ang II (Angiotensin II)

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1514-1525
Author(s):  
Anyun Ma ◽  
Lie Gao ◽  
Ahmed M. Wafi ◽  
Li Yu ◽  
Tara Rudebush ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Pressor Response ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Intracerebroventricular Infusion

We investigated the mechanism by which ACE2 (angiotensin-converting enzyme 2) overexpression alters neurohumoral outflow and central oxidative stress. Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is a master antioxidant transcription factor that regulates cytoprotective and antioxidant genes. We hypothesized that upregulation of central ACE2 inhibits the pressor response to Ang II (angiotensin II) by reducing reactive oxygen species through a Nrf2/antioxidant enzyme–mediated mechanism in the rostral ventrolateral medulla. Synapsin human Angiotensin Converting Enzyme 2 positive (SynhACE2 +/+ ) mice and their littermate controls synhACE2 −/− were used to evaluate the consequence of intracerebroventricular infusion of Ang II. In control mice, Ang II infusion evoked a significant increase in blood pressure and norepinephrine excretion, along with polydipsia and polyuria. The pressor effect of central Ang II was completely blocked in synhACE2 +/+ mice. Polydipsia, norepinephrine excretion, and markers of oxidative stress in response to central Ang II were also reduced in synhACE2 +/+ mice. The MasR (Mas receptor) agonist Ang 1–7 and blocker A779 had no effects on blood pressure. synhACE2 +/+ mice showed enhanced expression of Nrf2 in the rostral ventrolateral medulla which was blunted following Ang II infusion. Ang II evoked nuclear translocation of Nrf2 in cultured Neuro 2A (N2A) cells. In synhACE2 −/− mice, the central Ang II pressor response was attenuated by simultaneous intracerebroventricular infusion of the Nrf2 activator sulforaphane; blood pressure was enhanced by knockdown of Nrf2 in the rostral ventrolateral medulla in Nrf2 floxed (Nrf2 f/f ) mice. These data suggest that the hypertensive effects of intracerebroventricular Ang II are attenuated by selective overexpression of brain synhACE2 and may be mediated by Nrf2-upregulated antioxidant enzymes in the rostral ventrolateral medulla.

Tonic drive to sympathetic premotor neurons of rostral ventrolateral medulla from caudal pressor area neurons

1999 ◽  
Vol 276 (4) ◽  
pp. R1209-R1213 ◽  
Author(s):  
R. R. Campos ◽  
R. M. McAllen
Keyword(s):  
Blood Pressure ◽  
Significant Proportion ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Cervical Cord ◽  
Neuron Activity ◽  
Tonic Activity ◽  
Premotor Neurons ◽  
Sympathetic Premotor Neurons ◽  
Caudal Pressor

The responses of sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) to activation or inactivation of neurons in the caudal pressor area (CPA) were studied in urethan-anesthetized rats. Extracellular recordings were made from 32 barosensitive single units in the RVLM, of which 26 were antidromically activated from the cervical cord. Unilateral microinjections ofl-glutamate (0.5–5 nmol) into the CPA increased firing in 13 of 14 premotor neurons by 90 ± 30% while raising blood pressure. Both ipsilateral and contralateral injections were effective. Unilateral or bilateral inhibition of CPA neuron activity by microinjecting glycine (5–200 nmol/side) lowered blood pressure, while it reduced firing in 9 of 10 and 16 of 17 premotor neurons, respectively, by 45 ± 9 and 39 ± 6%. A significant proportion of tonic activity in RVLM sympathetic premotor neurons is thus driven, directly or indirectly, by neurons in the CPA.

scholarly journals Expression of Constitutively Active Angiotensin Receptors in the Rostral Ventrolateral Medulla Increases Blood Pressure

Hypertension ◽  
2006 ◽  
Vol 47 (6) ◽  
pp. 1054-1061 ◽  
Author(s):  
Andrew M. Allen ◽  
Jaspreet K. Dosanjh ◽  
Marco Erac ◽  
Sashikala Dassanayake ◽  
Ross D. Hannan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Angiotensin Receptors ◽  
Constitutively Active

Compression of the Rostral Ventrolateral Medulla by a Vagal Schwannoma of the Cerebellomedullary Cistern Presenting with Refractory Neurogenic Hypertension: Case Report

Neurosurgery ◽  
2006 ◽  
Vol 58 (6) ◽  
pp. E1212-E1212 ◽  
Author(s):  
Mahmoud H. Kamel ◽  
Nassir H. Mansour ◽  
Chris Mascott ◽  
Kristian Aquilina ◽  
Steven Young
Keyword(s):  
Blood Pressure ◽  
Case Report ◽  
Cranial Nerves ◽  
Pressure Control ◽  
Jugular Foramen ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Neurovascular Compression ◽  
Neurogenic Hypertension ◽  
First Case

Abstract OBJECTIVE: The rostral ventrolateral medulla is thought to serve as a final common pathway for the integration of central cardiovascular information and to be important for the mediation of central pressor responses. An association between essential hypertension and neurovascular compression of the rostral ventrolateral medulla has been reported. This may be mediated by an increase in sympathetic tone. CLINICAL PRESENTATION: Schwannomas arising from the lower cranial nerves (Cranial Nerves IX-XI) are rare, constituting only 3% of all intracranial schwannomas unassociated with neurofibromatosis. The majority of these tumors present as jugular foramen lesions and, less commonly, they occur along the extracranial course of these nerves. An intracisternal location is extremely rare. Fewer than 15 cases of pathologically proven intracisternal vagal schwannomas in the absence of neurofibromatosis have been reported. INTERVENTION: We report a case of vagal schwannoma in the cerebellomedullary cistern causing distortion of the vagal root entry zone and presenting with refractory neurogenic hypertension. Total microsurgical excision of this tumor, arising from one of the rootlets of the vagus nerve, was achieved. Immediately postoperatively, blood pressure decreased markedly, and despite our effort to maintain the blood pressure with fluids, the patient developed a cerebral infarction in the watershed zone. CONCLUSION: We discuss the proposed mechanism of hypertension, and the perioperative management, stressing blood pressure control. A review of the literature regarding vagal schwannomas is also presented. To the best of our knowledge, this is the first case report of a cerebellomedullary cistern vagal schwannoma presenting with neurogenic hypertension.

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