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.

Patterns of hemodynamic responses associated with central activation of coronary vasoconstriction

1992 ◽  
Vol 262 (2) ◽  
pp. R276-R283
Author(s):  
L. F. Jones ◽  
D. D. Gutterman ◽  
M. J. Brody
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Ventral Surface ◽  
Ventrolateral Medulla ◽  
Defense Reaction ◽  
Hemodynamic Responses ◽  
Coronary Vasoconstriction ◽  
Integrated Response ◽  
Coronary Vasoconstrictor

Previous studies in our laboratory have identified several central sites from which coronary vasoconstriction can be elicited by electrical stimulation. The present study was conducted to determine if specific patterns of hemodynamic responses are associated with activation of the coronary vasoconstrictor pathway in the hypothalamus, pons, and medulla. Cats anesthetized with chloralose were instrumented for recording arterial pressure, heart rate, and coronary, femoral, renal, and mesenteric blood flow velocities. After vagotomy and atenolol (1 mg/kg iv), anterior hypothalamus (AHA), parabrachial nucleus (PBN), a site very close to the ventral surface of the pons lateral to the pyramidal tract, and rostral ventrolateral medulla (RVLM) were stimulated electrically. Stimulation produced a decrease in coronary blood flow that was associated with all of the cardiovascular components of the defense reaction, an integrated response that included a decrease in hindquarter vascular resistance (blocked by methyl atropine), increases in renal and mesenteric vascular resistances, and a pressor response, except no change in renal vascular resistance from RVLM. Different patterns of hemodynamic responses were obtained from sites outside the coronary vasoconstrictor areas. From these results we conclude that coronary vasoconstriction is a frequent component of the defense reaction.

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.

Naloxone reverses inhibitory effect of electroacupuncture on sympathetic cardiovascular reflex responses

1999 ◽  
Vol 276 (6) ◽  
pp. H2127-H2134 ◽  
Author(s):  
Dong M. Chao ◽  
Lin L. Shen ◽  
Stephanie Tjen-A-Looi ◽  
Koullis F. Pitsillides ◽  
Peng Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Cardiovascular Reflex ◽  
Wide Range ◽  
Feline Model ◽  
Stimulation Of

Acupuncture and electroacupuncture (EA) have been used in traditional Chinese medicine to treat a wide range of diseases and conditions, including angina pectoris and myocardial infarction. In a feline model of reflex-induced reversible myocardial ischemia, electrical stimulation of the median nerves to mimic EA (Neiguan acupoint) significantly improved ischemic dysfunction, secondary to an inhibitory effect of EA on reflex pressor effects evoked by bradykinin (BK). The central mechanism of EA’s inhibitory effect in this model is unknown. Accordingly, in α-chloralose-anesthetized cats, BK (10 μg/ml) was applied to the gallbladder to elicit a cardiovascular reflex response that significantly ( P < 0.05) increased arterial blood pressure and heart rate; normalized systolic wall thickening (%WTh) of the left ventricle, measured by ultrasonic single-crystal sonomicrometer, increased by 31 ± 11% ( P < 0.05). After ligation of a side branch of the left anterior descending coronary artery, the reflex pressor response to BK resulted in a significant decrease of %WTh (−32 ± 6%) in the ischemic region. When bilateral EA of the Neiguan acupoints was performed, the pressor response to BK was inhibited and regional myocardial function was significantly improved (+19 ± 20%). The inhibitory effects of EA on blood pressure and %WTh were reversed by intravenous injection of naloxone (0.4 mg/kg; n = 9) or microinjection of naloxone (10 nM in 0.1 μl/site; n= 14) into the rostral ventrolateral medulla (rVLM). Thus %WTh with intravenous naloxone was reduced to −13 ± 29% ( P<0.05) during stimulation of the gallbladder. Our results indicate that the inhibitory effect of EA on the BK-induced pressor response and the consequent improvement of ischemic dysfunction is dependent on the activation of opioid receptors, specifically receptors located in the rVLM.

Cardiovascular effects of opioid antagonist naloxone in rostral ventrolateral medulla of rabbits

1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers
Keyword(s):  
Pressor Response ◽  
Cardiovascular Effects ◽  
Rostral Ventrolateral Medulla ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Beneficial Effects ◽  
Arterial Blood ◽  
Depressor Effect

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.

scholarly journals Superoxide scavenging in the rostral ventrolateral medulla blunts the pressor response to peripheral chemoreflex activation

2010 ◽  
Vol 1351 ◽  
pp. 141-149 ◽  
Author(s):  
Fabíola C. Nunes ◽  
Thaís P. Ribeiro ◽  
Maria S. França-Silva ◽  
Isac A. Medeiros ◽  
Valdir A. Braga
Keyword(s):  
Pressor Response ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Peripheral Chemoreflex

Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Single Unit Activity ◽  
Afferent Pathways ◽  
Sympathetic Control ◽  
Stellate Ganglia ◽  
Cervical Vagotomy ◽  
The Mean ◽  
Cardiac Receptors ◽  
Stimulation Of

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.

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