scholarly journals Baroreceptor-vasomotor reflex after N-methyl-D-aspartate receptor blockade in rabbit caudal ventrolateral medulla.

1989 ◽  
Vol 416 (1) ◽  
pp. 67-78 ◽  
Author(s):  
W W Blessing
Keyword(s):  
Ventrolateral Medulla ◽  
Receptor Blockade ◽  
Caudal Ventrolateral Medulla ◽  
Aspartate Receptor ◽  
Vasomotor Reflex

Lesion of the caudal ventrolateral medulla prevents the induction of hypertension by adenosine receptor blockade in rats

2006 ◽  
Vol 1073-1074 ◽  
pp. 374-382 ◽  
Author(s):  
Dora Pinho ◽  
Teresa Sousa ◽  
Manuela Morato ◽  
Isaura Tavares ◽  
António Albino-Teixeira
Keyword(s):  
Adenosine Receptor ◽  
Ventrolateral Medulla ◽  
Receptor Blockade ◽  
Caudal Ventrolateral Medulla

Depressor neurons in rabbit caudal medulla do not transmit the baroreceptor-vasomotor reflex

1987 ◽  
Vol 253 (4) ◽  
pp. H777-H786 ◽  
Author(s):  
W. W. Blessing ◽  
J. O. Willoughby
Keyword(s):  
Arterial Pressure ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Caudal Ventrolateral Medulla ◽  
Depressor Response ◽  
Renal Nerve Activity ◽  
Electrolytic Lesions ◽  
Vasomotor Reflex

Experiments to determine whether depressor neurons in the caudal ventrolateral medulla form an integral part of the central pathway transmitting the baroreceptor-vasomotor reflex were performed on rabbits anesthetized with urethan. The function of the depressor neurons was altered by intramedullary injections of agents that stimulate or block receptors for gamma-aminobutyric acid and by electrolytic lesions in the caudal ventrolateral medulla. Muscimol abolished both the depressor response and the inhibition of renal nerve activity normally observed after stimulation of the aortic depressor nerve and caused a paradoxical reversal of the depressor response. However, muscimol only partially impaired the inhibition of renal nerve activity produced by experimental elevation of arterial pressure, and it did not affect the increase in renal nerve activity normally produced by decreasing arterial pressure. Bicuculline methiodide amplified the depressor response and the inhibition of renal nerve activity and also restored baroreceptor-vasomotor reflexes abolished by muscimol. Bilateral electrolytic lesions did not alter any component of the baroreceptor-vasomotor reflex. Results indicate that the depressor neurons in the caudal ventrolateral medulla do not form an integral part of the central pathway mediating the baroreceptor-vasomotor reflex. However, output from the depressor neurons appears to inhibit sympathoexcitatory neurons, which also receive baroreceptor-derived inhibitory inputs.

Contribution of α2-adrenoceptors in caudal ventrolateral medulla to cardiovascular regulation in rat

1998 ◽  
Vol 274 (4) ◽  
pp. R1119-R1124 ◽  
Author(s):  
Shogo Sesoko ◽  
Hiromi Muratani ◽  
Masanobu Yamazato ◽  
Hiroshi Teruya ◽  
Shuichi Takishita ◽  
...  
Keyword(s):  
Cardiovascular Effect ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
Renal Sympathetic Nerve Activity ◽  
Caudal Ventrolateral Medulla ◽  
Adrenoceptor Antagonist ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid ◽  
Cardiovascular Neurons ◽  
Selective Blocker

The inhibitory action of α2-agonists on the cardiovascular neurons has been elucidated in the rostral ventrolateral medulla (RVLM) but not in the caudal ventrolateral medulla (CVLM). Our study aimed to clarify whether microinjection of clonidine into the CVLM elicits any cardiovascular effect and whether endogenous α2-adrenoceptor-mediated mechanisms contribute to the tonic activity of the CVLM neurons. In male Sprague-Dawley rats (7–9 wk old, 270–320 g) anesthetized with urethan, unilateral microinjection of 8 nmol of clonidine into the CVLM ( n = 10) increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) by 12.1 ± 1.8 mmHg (mean ± SE, P < 0.01) and 25.8 ± 4.8% ( P < 0.01), while heart rate (HR) remained unaltered. Unilateral microinjection of 2 nmol of SKF-86466, a selective blocker of the α2-adrenoceptors, into the CVLM ( n = 10) decreased MAP, HR, and RSNA (−11.6 ± 2.6 mmHg, −26 ± 7 beats/min, and −15.3 ± 1.7%, respectively, P < 0.01 for each). Artificial cerebrospinal fluid caused neither a cardiovascular effect nor a sympathetic response. Prior injection of SKF-86466 into the ipsilateral CVLM attenuated the effects of clonidine. Bilateral microinjection of muscimol into the RVLM abolished the effects of both clonidine and SKF-86466 injected into the CVLM. The pressor and sympathoexcitatory effects of clonidine injected into the CVLM suggest a neuroinhibitory action of the drug on the CVLM neurons. In addition,the depressor and sympathoinhibitory effects of SKF-86466 injected into the CVLM indicated that activation of α2-adrenoceptors by endogenous ligand inhibits CVLM neurons. The effects of clonidine and the α2-adrenoceptor antagonist in the CVLM require the integrity of the RVLM.

scholarly journals Altered regulation of the rostral ventrolateral medulla in hypertensive obese Zucker rats

2011 ◽  
Vol 301 (1) ◽  
pp. H230-H240 ◽  
Author(s):  
Domitila A. Huber ◽  
Ann M. Schreihofer
Keyword(s):  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Input ◽  
Rostral Ventrolateral Medulla ◽  
Male Rats ◽  
Ventrolateral Medulla ◽  
Zucker Rats ◽  
Caudal Ventrolateral Medulla ◽  
Obese Zucker Rats ◽  
Altered Regulation

Obese Zucker rats (OZR) have elevated sympathetic nerve activity (SNA) and mean arterial pressure (MAP) compared with lean Zucker rats (LZR). We examined whether altered tonic glutamatergic, angiotensinergic, or GABAergic inputs to the rostral ventrolateral medulla (RVLM) contribute to elevated SNA and MAP in OZR. Male rats (14–18 wk) were anesthetized with urethane (1.5 g/kg iv), ventilated, and paralyzed to record splanchnic SNA, heart rate (HR), and MAP. Inhibition of the RVLM by microinjections of muscimol eliminated SNA and evoked greater decreases in MAP in OZR vs. LZR ( P < 0.05). Antagonism of angiotensin AT1 receptors in RVLM with losartan yielded modest decreases in SNA and MAP in OZR but not LZR ( P < 0.05). However, antagonism of ionotropic glutamate receptors in RVLM with kynurenate produced comparable decreases in SNA, HR, and MAP in OZR and LZR. Antagonism of GABAA receptors in RVLM with gabazine evoked smaller rises in SNA, HR, and MAP in OZR vs. LZR ( P < 0.05), whereas responses to microinjections of GABA into RVLM were comparable. Inhibition of the caudal ventrolateral medulla, a major source of GABA to the RVLM, evoked attenuated rises in SNA and HR in OZR ( P <0.05). Likewise, inhibition of nucleus tractus solitarius, the major excitatory input to caudal ventrolateral medulla, produced smaller rises in SNA and HR in OZR. These results suggest the elevated SNA and MAP in OZR is derived from the RVLM and that enhanced angiotensinergic activation and reduced GABAergic inhibition of the RVLM may contribute to the elevated SNA and MAP in the OZR.

Excitatory somato-sympathetic reflexes are relayed in the caudal ventrolateral medulla in the cat

1994 ◽  
Vol 179 (1-2) ◽  
pp. 71-74 ◽  
Author(s):  
Johannes Zanzinger ◽  
Jens Doutheil ◽  
Jürgen Czachurski ◽  
Horst Seller
Keyword(s):  
Ventrolateral Medulla ◽  
Caudal Ventrolateral Medulla ◽  
Sympathetic Reflexes
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