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 the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

Respiratory responses to aortic and carotid chemoreceptor activation in the dog

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku
Keyword(s):  
Electrical Stimulation ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Chemical Stimulation ◽  
Respiratory Drive ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Respiratory Reflexes ◽  
Respiratory Responses ◽  
Stimulation Of

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.

Effect of Large Doses of Head Irradiation in Dogs

1958 ◽  
Vol 194 (2) ◽  
pp. 344-350 ◽  
Author(s):  
Ming-Tsung Peng ◽  
Shu Chien ◽  
Magnus I. Gregersen
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Respiratory Rate ◽  
Cause Of Death ◽  
Carotid Sinus ◽  
Pressor Response ◽  
Respiratory Response ◽  
Neurological Signs ◽  
X Irradiation

Dogs in which the head was x-irradiated with 23,500 r survived from 14 to 28 hours. The chief neurological signs were disturbance of equilibrium and extensor rigidity. Throughout the whole postirradiation course, the blood volume showed very little change. Arterial pressure, heart rate and respiratory rate remained essentially unchanged until about 1 hour before death. The carotid sinus reflex did not change until 30–60 minutes before death, but then deteriorated rapidly. Generally, the respiratory response to cyanide injection was still present after the disappearance of the carotid sinus reflex. At the terminal stage, the pressor response of the medullary vasomotor center to electrical stimulation decreased in parallel to that of the carotid sinus reflex. The vital centers in the medulla oblongata are directly damaged by large doses of x-irradiation. The failure of respiration is the cause of death.

Inhibition of renal sympathetic nervous activity by area postrema stimulation in rabbits

1987 ◽  
Vol 253 (1) ◽  
pp. H91-H99 ◽  
Author(s):  
E. M. Hasser ◽  
D. O. Nelson ◽  
J. R. Haywood ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Consistent Change ◽  
Renal Sympathetic ◽  
Stimulation Of

This study investigated the effect of chemical and electrical stimulation of the area postrema on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate in urethan-anesthetized rabbits. Electrical stimulation of the area postrema at 2, 5, 10, 20, 40, and 80 Hz using constant currents of 7.5, 15, and 30 microA (pulse duration = 0.3 ms, train duration = 5 s) produced progressive decreases in RSNA and heart rate, with no consistent change in arterial pressure. To control for electrical activation of fibers of passage in or near the area postrema, L-glutamate was injected into the area postrema using glass micropipettes. Micropressure injection of L-glutamate (10 mM) in volumes of 5-10 nl produced rapid decreases in RSNA averaging 27 +/- 5% (P less than 0.05) accompanied by a small bradycardia. The effects of electrical stimulation of the area postrema, but not the adjacent nucleus tractus solitarius, were totally eliminated by micropressure injection of kainic acid (40 ng in 40 nl) into the area postrema. During continuous electrical stimulation of the area postrema using parameters that produced small decrements in RSNA and heart rate, the slope of the line relating baroreflex inhibition of RSNA to increases in arterial pressure during graded infusions of phenylephrine was significantly enhanced (-6.77 +/- 1.30 vs. -3.81 +/- 0.66% RSNA/mmHg). These data are consistent with the hypothesis that activation of neurons in the area postrema results in an inhibition of RSNA. Furthermore, stimulation of the area postrema augments baroreflex inhibition of RSNA during increases in arterial pressure with phenylephrine.

Effect of indomethacin on the pressor responses to sustained isometric contraction in humans

1993 ◽  
Vol 75 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K. P. Davy ◽  
W. G. Herbert ◽  
J. H. Williams
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Muscle Ischemia ◽  
Stimulation Of

The purpose of this study was to test the hypothesis that prostaglandins participate in metaboreceptor stimulation of the pressor response to sustained isometric handgrip contraction in humans. To accomplish this, mean arterial pressure, heart rate (n = 10), and plasma norepinephrine levels (n = 8) were measured in healthy male subjects during sustained isometric handgrip at 40% of maximal voluntary contraction force to exhaustion and during a period of postcontraction muscle ischemia. The subjects were given a double-blind and counterbalanced administration of placebo or a single 100-mg dose of indomethacin. A period of 1 wk was allowed for systemic clearance of the drug. Mean arterial pressure increased 25 +/- 5 vs. 22 +/- 4 mmHg during the final minute of isometric handgrip contraction and 26 +/- 2 vs. 21 +/- 5 during the last minute of postcontraction muscle ischemia in the placebo vs. the indomethacin trial (P > 0.05), respectively. Heart rate was increased 21 +/- 4 vs. 17 +/- 3 beats/min during the final minute of isometric handgrip contraction in the placebo vs. the indomethacin trial (P > 0.05), respectively, and returned to control values during postcontraction muscle ischemia. Plasma norepinephrine levels increased 343 +/- 89 vs. 289 +/- 89 pg/ml after isometric handgrip contraction and 675 +/- 132 vs. 632 +/- 132 pg/ml after postcontraction muscle ischemia (P > 0.05) in the placebo vs. the indomethacin trial, respectively. These results suggest that prostaglandin inhibition does not significantly modulate muscle contraction-induced stimulation of mean arterial pressure, heart rate, or plasma norepinephrine levels.

Effect of paraventricular nucleus lesions on cardiovascular responses elicited by stimulation of the subfornical organ in the rat

1985 ◽  
Vol 63 (7) ◽  
pp. 816-824 ◽  
Author(s):  
Michael B. Gutman ◽  
John Ciriello ◽  
Gordon J. Mogenson
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Subfornical Organ ◽  
Short Latency ◽  
Peak Latency ◽  
Ganglionic Blockade ◽  
Stimulation Of

It has recently been reported that stimulation of the region of the subfornical organ (SFO) elicits an increase in arterial pressure. However, the mechanisms and forebrain neural circuitry that are involved in this cardiovascular response have not been elucidated. The present study was done in urethane-anaesthetized rats to determine whether selective activation of SFO neurons elicit cardiovascular responses and whether these responses were mediated by a pathway involving the paraventricular nucleus of the hypothalamus (PVH). Stimulation sites which required the lowest threshold current (30 μA) to elicit a pressor response and at which the largest rise in mean arterial pressure (MAP; 22 ± 2 mmHg) was elicited at a constant current intensity (150 μA) were histologically localized in the region of the SFO. Short (mean peak latency; 4 ± 2 s) and long (mean peak latency; 61 ± 8 s) latency increases in MAP were observed during and after electrical stimulation of the SFO, respectively. Cardiac slowing accompanied the short latency pressor response and cardioacceleration was observed in most (57%) of the cases to accompany the late pressor response. Microinjection of L-glutamate into the SFO consistently elicited cardiovascular responses qualitatively similar to those observed during electrical stimulation. Ganglionic blockade abolished the short latency increase in MAP and the accompanying bradycardia. However, the long latency pressor and cardioacceleratory responses were not altered by ganglionic blockade and adrenalectomy. Selective bilateral electrolytic or kainic acid lesions of the region of the PVH significantly attenuated the cardiovascular responses elicited by stimulation of the SFO. These data suggest that activation of neurons in the SFO elicit cardiovascular responses partially mediated by sympathetic outflow through a neural pathway involving the PVH.

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.

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