Axons of passage may be responsible for fastigial nucleus pressor response

1989 ◽  
Vol 257 (6) ◽  
pp. R1436-R1440
Author(s):  
R. T. Henry ◽  
J. D. Connor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Kainic Acid ◽  
Pulse Width ◽  
Pressor Response ◽  
Fastigial Nucleus ◽  
Postural Asymmetry ◽  
Bilateral Destruction ◽  
Stimulation Of

Bilateral destruction of perikarya in the fastigial nucleus (FN) of the rat with the cytotoxic agent kainic acid (0.5 mg) did not alter the blood pressure (BP) increases observed during monopolar electrical stimulation (100 microA, 50 Hz, 0.5-ms pulse width) of this region. BP increases in control animals were 30 +/- 8 mm Hg, whereas BP increased 30 +/- 7 mmHg in kainic acid-lesioned rats. Furthermore, picrotoxin (100 ng) and muscimol (25 ng) microinjected unilaterally into the FN of conscious, unrestrained rats produced postural asymmetry but no change in BP or heart rate. These data suggest that the FN pressor response may be due, at least in part, to stimulation of axons of passage.

Fastigial nucleus cardiovascular response and brain stem lesions in the beagle

1986 ◽  
Vol 250 (2) ◽  
pp. H231-H239 ◽  
Author(s):  
K. J. Dormer ◽  
J. A. Andrezik ◽  
R. J. Person ◽  
J. T. Braggio ◽  
R. D. Foreman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Kainic Acid ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Fastigial Nucleus ◽  
Reticular Nucleus ◽  
A5 Area

Changes in the excitatory cardiovascular response (heart rate, arterial blood pressure, left ventricular pressure, and LV dP/dt as an index of myocardial contractility) resulting from electrical stimulation of the cerebellar fastigial nucleus (FN) were recorded after placement of DC or radio-frequency lesions or after microinjections of kainic acid into brain stem areas that receive FN projections and have been shown to be involved in central cardiovascular control. FN-induced increases in heart rate, blood pressure, and contractility were reduced or abolished by lesions made in the restiform body or the A5 area, which is homologous to the catecholamine-containing region in cats and rats. Lesions in the paramedian reticular nucleus, rostral and caudal to obex, failed to reduce the FN cardiovascular response. Nucleus of the solitary tract lesions augmented the FN pressor response and tachycardia. Kainic acid (1 microliter of 100 mM solution) caused profound depression of heart rate, blood pressure, and contractility and reduced or eliminated the FN-induced cardiovascular response when injected into the A5 area, previously identified by the pressor response following electrical stimulation. We concluded from these observations that a descending fastigiobulbar sympathoexcitatory pathway courses through a previously identified A5 pressor area that is also capable of a depressor response when the cell bodies alone are activated.

Stimulation of parabrachial neurons elicits a sympathetically mediated pressor response in cats

1988 ◽  
Vol 255 (6) ◽  
pp. H1349-H1358 ◽  
Author(s):  
J. S. Hade ◽  
S. W. Mifflin ◽  
T. S. Donta ◽  
R. B. Felder
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Electrical Stimulus ◽  
Respiratory Drive ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Low Intensity ◽  
Stimulation Of

We examined the role of the parabrachial neuronal mass in mediating the pressor response to electrical stimulation of parabrachial nucleus (PBN). In anesthetized cats, 100 mM L-glutamate (L-glu) was microinjected into PBN at sites from which low-intensity (25 microA) electrical stimulation evoked a pressor response. Arterial pressure, heart rate, and, in some animals, renal or phrenic nerve activity were monitored. Microinjection of L-glu caused an increase in arterial pressure that was comparable with that elicited by low-intensity electrical stimulation. Electrical stimulation, and to a lesser extent L-glu microinjection, caused an increase in renal sympathetic nerve activity but no significant change in heart rate. No consistent change in central respiratory drive accompanied the pressor response. These responses were preserved after baroreceptor denervation but were blocked by intravenous administration of the alpha-adrenergic receptor antagonist phentolamine. Microinjection into PBN of 2 mM kainic acid, which selectively depolarizes neurons but spares axons, reversibly blocked the arterial pressure and renal nerve responses to the 25-microA electrical stimulus. We conclude that the pressor response elicited by electrical stimulation of PBN in the anesthetized cat is mediated by cellular elements in PBN, not by fibers of passage. Because phentolamine completely blocked the pressor response, we suggest that it is subserved peripherally by sympathetic alpha-adrenergic rather than humoral (e.g., angiotensin, vasopressin) vasoconstrictor mechanisms. Finally, our data indirectly suggest that PBN stimulation may differentially engage efferent components of the sympathetic nervous system to elicit the pressor response.

Fastigial stimulation releases vasopressin in amounts that elevate arterial pressure

1983 ◽  
Vol 244 (5) ◽  
pp. H687-H694 ◽  
Author(s):  
A. Del Bo ◽  
A. F. Sved ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Stimulus Train ◽  
Specific Antagonist ◽  
6 Hydroxydopamine ◽  
Stimulation Of ◽  
Intact Rats

Electrical stimulation of the cerebellar fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rat with a 10-s stimulus train (50 Hz) resulted in a stimulus-locked elevation in arterial pressure (AP) and heart rate, the fastigial pressor response (FPR). Blockade of autonomic effectors by chemosympathectomy (produced by treatment with 6-hydroxydopamine) combined with adrenalectomy, or by spinal cord transection at C1, abolished the FPR but unmasked an elevation of AP with longer latency (10-12 s) and duration (2-4 min), termed the residual FPR. The residual FPR was 1) abolished by midbrain transection, 2) blocked by administration of a specific antagonist of the vasopressor response to arginine vasopressin (AVP) [1,d(CH2)5Tyr(Me)AVP], and 3) was absent in homozygous and attenuated in heterozygous rats of the Brattleboro strain. FN stimulation elevated AVP threefold (from 13 +/- 1 to 38 +/- 8 pg/ml, P less than 0.02; n = 6) in intact rats and sevenfold in rats with combined chemosympathectomy and adrenalectomy (from 14 +/- 1 to 96 +/- 11 pg/ml, P less than 0.001; n = 9). Stimulation of the cerebellar FN can release AVP. In the absence of sympathoadrenal effectors, the amount so released is enhanced and capable of elevating AP.

Electrical Stimulation of Vascular Autonomic Nerves: Effects on Heart Rate, Blood Pressure, and Arrhythmias

2015 ◽  
Vol 38 (7) ◽  
pp. 825-830 ◽  
Author(s):  
JIAN SUN ◽  
BENJAMIN J. SCHERLAG ◽  
BO HE ◽  
XIAOHUA SHEN ◽  
MEI GAO ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Autonomic Nerves ◽  
Stimulation Of

scholarly journals Electrical stimulation of the midbrain increases heart rate and arterial blood pressure in awake humans

2002 ◽  
Vol 539 (2) ◽  
pp. 615-621 ◽  
Author(s):  
Judith M. Thornton ◽  
Tipu Aziz ◽  
David Schlugman ◽  
David J. Paterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Stimulation Of

Effects of electrical stimulation of the pontine A5 cell group on blood pressure and heart rate in the rabbit

1986 ◽  
Vol 379 (1) ◽  
pp. 10-23 ◽  
Author(s):  
Michael L. Woodruff ◽  
Ronald H. Baisden ◽  
Dennis L. Whittington
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Cell Group ◽  
Stimulation Of

A model of dynamic exercise: the decerebrate rat locomotor preparation

1992 ◽  
Vol 72 (1) ◽  
pp. 121-127 ◽  
Author(s):  
T. G. Bedford ◽  
P. K. Loi ◽  
C. C. Crandall
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Pressure Response ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Decerebrate Rat ◽  
Stimulation Of

The purpose of this study was to develop a dynamic exercise model in the rat that could be used to study central nervous system control of the cardiovascular system. Rats of both sexes were decerebrated under halothane anesthesia and prepared for induced locomotion on a freely turning wheel. Electrical stimulation of the mesencephalic locomotor region (MLR) elicited locomotion at different speeds and gait patterns and increased heart rate and blood pressure. Two maneuvers were performed to illustrate the potential use of the preparation. The first maneuver consisted of muscular paralysis, which prevents excitation of muscle mechanoreceptors and chemoreceptors resulting from exercise. MLR stimulation still increased blood pressure. The second maneuver was performed to determine whether the blood pressure response obtained during paralysis was an artifact of electrical stimulation of the MLR. After microinjection of gamma-aminobutyric acid into the MLR, electrical current thresholds for blood pressure and locomotion increased in parallel. gamma-Aminobutyric acid injection also reduced the pressor response to suprathreshold electrical stimulation by 76%. The injection results suggest that electrical stimulation of the MLR activates cells rather than fibers of passage. The blood pressure response of the exercise model is probably not an artifact of stimulation. The decerebrate rat locomotor preparation should offer another approach to investigate difficult problems in exercise physiology.

Sympathetic alterations after midline medullary raphe lesions

1987 ◽  
Vol 253 (1) ◽  
pp. R91-R100 ◽  
Author(s):  
R. B. McCall ◽  
L. T. Harris
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Vagal Afferents ◽  
Nerve Activity ◽  
Medullary Raphe ◽  
Stimulation Of

The present study was designed to determine the functional importance of the midline medullary raphe nuclei in the autonomic regulation of the cardiovascular system in the anesthetized cat. Baroreceptor and somatosympathetic reflexes as well as the effects of electrical stimulation of vagal afferents and pressor and depressor sites in the hypothalamus and spinal trigeminal tract were determined before and after midline medullary lesions that extended from 2 to 7 mm rostral to the obex. Midline medullary lesions failed to affect baroreceptor reflexes as judged by the lack of effect on the sympathoinhibition associated with the pressor response to phenylephrine and the degree of slow-wave locking of sympathetic activity to the cardiac cycle. However, the lesion did significantly increase spontaneous sympathetic activity recorded from the inferior cardiac nerve. Blood pressure and heart rate were not altered by midline lesions. In addition, the computer-summed sympathoexcitatory response to electrical stimulation of somatic afferents in the sciatic nerve and the sympathoinhibitory response to stimulation of vagal afferent fibers were not affected by midline lesions. In contrast, the decrease in blood pressure and inhibition of sympathetic nerve activity elicited by electrical stimulation of the spinal trigeminal tract were completely abolished by the lesion. Depressor responses evoked from the anteroventral third ventricle region of the hypothalamus but not pressor responses elicited from the posterior hypothalamus were eliminated following midline medullary lesions. Finally, the sympathoinhibitory actions of the serotonin antagonist methysergide were blocked by medullary raphe lesions. These data indicate that neural elements in the medial medullary area function to provide a tonic inhibition of sympathetic nerve activity that is of nonbaroreceptor origin. Depressor responses evoked from the anterior hypothalamus and the spinal trigeminal tract also are mediated through this area of the medulla. Finally, the data support our contention that medullary serotonergic neurons have a sympathoexcitatory function.

Pressor responses and adrenomedullary catecholamine release during brain stimulation in the rat

1981 ◽  
Vol 59 (5) ◽  
pp. 485-492 ◽  
Author(s):  
Pierre Gauthier
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Brain Stimulation ◽  
Active Sites ◽  
Pressor Response ◽  
Secondary Phase ◽  
Plasma Catecholamine ◽  
Central Gray Matter ◽  
Central Gray ◽  
Stimulation Of

Electrical stimulation of the diencephalon and rostral mesencephalon produced a biphasic pressor response consisting of an initial sharp rise followed by a more prolonged elevation in blood pressure. Active sites from which comparable responses could be evoked were found in the ventral medial and lateral hypothalamus, in the region of the parafascicularis nucleus, and in the central gray matter and the tegmentum of the mesencephalon. Together with the biphasic pressor response brain stimulation also increased plasma catecholamine (CA) concentrations 10-fold. Either bilateral adrenalectomy or demedullation selectively abolished the secondary phase of the pressor response and greatly reduced the plasma CA response to stimulation. After chemical destruction of the terminals of the sympathetic neurones by intravenous administration of 6-hydroxydopamine (6-OHDA), the primary pressor phase was eliminated whereas the secondary phase as well as plasma CA concentration reached higher levels than in normal rats. 6-OHDA treatment combined with adrenalectomy completely abolished both pressor and CA responses. The results demonstrate that adrenomedullary mechanisms capable of increasing blood pressure significantly can be activiated by electrical stimulation of different sites in the diencephalon and mesencephalon.

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