scholarly journals Rostral ventrolateral medulla regulates pancreatic and gastric blood flow

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Anthony J.M. Verberne ◽  
Kathleen M McInerney
Keyword(s):  
Blood Flow ◽  
Rostral Ventrolateral Medulla ◽  
Gastric Blood Flow ◽  
Ventrolateral Medulla

Characterization of coronary vasoconstriction produced by rostral ventrolateral medulla stimulation in rats

1992 ◽  
Vol 262 (2) ◽  
pp. H437-H442 ◽  
Author(s):  
L. F. Jones ◽  
M. J. Brody
Keyword(s):  
Blood Flow ◽  
Rat Model ◽  
Pressor Response ◽  
Sympathetic Innervation ◽  
Inhibitory Effect ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Coronary Vasoconstriction ◽  
Stimulation Of

Previous studies have demonstrated that coronary vasoconstriction can be produced by activation of specific central nervous system sites in the cat. The present study was undertaken 1) to develop a rat model for studying central influences on coronary circulation and 2) to utilize this model for characterization of the changes in coronary blood flow (CBF) produced by stimulation of rostral ventrolateral medulla (RVLM). Electrical stimulation of right RVLM in chloralose-anesthetized rats with bilateral vagotomy produced a transient decrease in CBF followed by an increase in CBF concomitant with a decrease in hindquarter blood flow, a pressor response, and tachycardia. After atenolol the tachycardia and increase in CBF were abolished, whereas the decrease in CBF was enhanced and prolonged. Phentolamine (1 mg/kg iv) or removal of the stellate ganglia inhibited the decrease in CBF but did not totally abolish the increase in coronary vascular resistance. Inhibition of nitric oxide synthesis with N-nitro-L-arginine (10 microM/kg iv) enhanced the decrease in CBF produced by stimulation in RVLM. These results indicate that, in rat model, the centrally induced decrease in CBF is 1) mediated by cardiac sympathetic innervation but only partially through alpha-adrenoceptors and 2) enhanced by removal of the inhibitory effect of the endothelium.

scholarly journals Nitric Oxide and Prostanoids Participate in Cerebral Vasodilation Elicited by Electrical Stimulation of the Rostral Ventrolateral Medulla

1994 ◽  
Vol 14 (3) ◽  
pp. 492-502 ◽  
Author(s):  
Eugene V. Golanov ◽  
Donald J. Reis
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Electrical Stimulation ◽  
Cerebral Arteries ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Doppler Flowmetry ◽  
Cerebral Vasodilation ◽  
The Brain ◽  
Stimulation Of

We investigated, using laser-Doppler flowmetry, whether nitric oxide (NO)- and/or indomethacin (IND)-sensitive mechanisms mediate the elevations of regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral ventrolateral medulla (RVL) in the anesthetized spinalized rat. Stimulation of the RVL for 10 s caused increased rCBF in the frontal cortex by 31% ( n = 46), peaking at 22 s and persisting for up to 8 min. Intravenous l-nitro- NG-arginine (NNA) dose dependently and reversibly increased arterial pressure and reduced basal and evoked rCBF to 74 and 54% of the control, respectively ( p < 0.05; n = 7). Superfused over the cortex, NNA dose dependently reduced only the evoked elevations of rCBF, to 39% of the control ( p < 0.05; n = 6). Intravenous IND decreased the basal rCBF dose dependently and decreased the elevations evoked from the RVL by 38% ( p < 0.05), but IND was without effect when superfused. Combined, the effects of intravenous NNA and IND summated, reducing rCBF by 70%. However, when NNA and IND were superfused together, the inhibition of the evoked vasodilation was comparable to that elicited by NNA alone. We conclude that the elevation in rCBF elicited from the RVL is partially mediated by (a) NO synthesized locally in the cortex in response to an afferent neural signal and (b) an IND-sensitive mechanism, probably a product of cyclooxygenase, located in larger cerebral arteries, in response to a retrograde vascular signal resulting from increased blood flow within the brain.

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