Differential drives from rostral ventrolateral medullary neurons to three identified sympathetic outflows

1994 ◽  
Vol 267 (4) ◽  
pp. R935-R944 ◽  
Author(s):  
R. M. McAllen ◽  
C. N. May

Simultaneous recordings were made in chloralose-anesthetized cats from muscle vasoconstrictor (MVC), visceral vasoconstrictor (VVC), and renal (RSN) sympathetic fibers. Their barosensitivity was demonstrated, after which all baroreceptor nerves were cut. Multiple microinjections of sodium glutamate (5 nl, 0.1 M) were made in a grid pattern covering the rostral ventrolateral medulla (RVLM) pressor area on seven sides of four animals. Injections increased blood pressure by up to 87 +/- 22 mmHg and MVC, VVC, and RSN activities by up to 169 +/- 55, 62 +/- 23, and 67 +/- 36%, respectively. The relative responses between nerves (taken in pairs) showed significant inhomogeneity across injections into 5/7, 6/7, and 1/7 RVLMs for MVC vs. VVC, MVC vs. RSN, and VVC vs. RSN, respectively. Calculation showed that overall, less than half the response spikes due to RVLM glutamate injections could be accounted for by a hypothetical population of neurons that excited MVC, VVC, and RSN outflows in fixed proportion. Sites that exclusively drove MVC, VVC, or RSN outflows were found in 7/7, 3/7, and 5/7 RVLMs, respectively. Sites that selectively drove either nerve of a given pair were ubiquitous. The RVLM territories from which the three outflows could be activated overlapped but showed clear differences. Their shapes and sizes differed between animals and even between sides. They covered the subretrofacial (SRF) nucleus plus a variable rostromedial extension. The data support the view that the RVLM neurons driving these three sympathetic outflows are largely, perhaps entirely, separate populations.

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1514-1525
Author(s):  
Anyun Ma ◽  
Lie Gao ◽  
Ahmed M. Wafi ◽  
Li Yu ◽  
Tara Rudebush ◽  
...  

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.


2000 ◽  
Vol 278 (3) ◽  
pp. R692-R697 ◽  
Author(s):  
Chiung-Tong Chen ◽  
Ling-Ling Hwang ◽  
Jaw-Kang Chang ◽  
Nae J. Dun

Orexin A and B, two recently isolated hypothalamic peptides, have been reported to increase food consumption upon intracerebroventricular injections in rats. In addition to the hypothalamus, orexin A-immunoreactive fibers have been observed in several areas of the medulla that are associated with cardiovascular functions. The present study was undertaken to evaluate the hypothesis that orexins may influence cardiovascular response by interacting with neurons in the medulla. Intracisternal injections of orexins A (0.0056–7.0 nmol) or B (0.028–0.28 nmol) dose dependently increased mean arterial pressure (MAP) by 4–27 mmHg and heart rate (HR) by 26–80 beats/min in urethan-anesthetized rats, with orexin A being more effective in this regard. MAP and HR were not changed by intravenous injection of orexins at higher concentrations. Microinjection of orexin A (14 pmol/50.6 nl) to the rostral ventrolateral medulla, which was confirmed by histological examination, increased MAP and HR. Our results indicate that, in addition to a role in positive feeding behavior, orexins may enhance cardiovascular response via an action on medullary neurons.


1999 ◽  
Vol 276 (4) ◽  
pp. R1209-R1213 ◽  
Author(s):  
R. R. Campos ◽  
R. M. McAllen

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.


Hypertension ◽  
2006 ◽  
Vol 47 (6) ◽  
pp. 1054-1061 ◽  
Author(s):  
Andrew M. Allen ◽  
Jaspreet K. Dosanjh ◽  
Marco Erac ◽  
Sashikala Dassanayake ◽  
Ross D. Hannan ◽  
...  

Neurosurgery ◽  
2006 ◽  
Vol 58 (6) ◽  
pp. E1212-E1212 ◽  
Author(s):  
Mahmoud H. Kamel ◽  
Nassir H. Mansour ◽  
Chris Mascott ◽  
Kristian Aquilina ◽  
Steven Young

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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