Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

Rostral ventrolateral medullary opioid receptor activation modulates pressor response to muscle contraction

1998 ◽  
Vol 274 (1) ◽  
pp. H139-H146 ◽  
Author(s):  
Daryl Caringi ◽  
David J. Mokler ◽  
David M. Koester ◽  
Ahmmed Ally
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Tibial Nerve Stimulation ◽  
Isometric Muscle Contraction ◽  
Isometric Muscle

The effects of an opioid agonist, [d-Ala2]methionine enkephalinamide (DAME), administered into the rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses to isometric muscle contraction were determined in anesthetized rats. A 30-s contraction evoked by tibial nerve stimulation increased mean arterial pressure (MAP) and heart rate (HR) by 34 ± 6 mmHg and 40 ± 7 beats/min, respectively, with a developed tension of 322 ± 30 g, after bilateral insertion of microdialysis probes into the rVLM. Thirty-minute dialysis of DAME (10 and 100 μM) attenuated the contraction-evoked cardiovascular changes dose dependently (10 μM: MAP = 25 ± 4 mmHg, HR = 27 ± 3 beats/min, tension = 333 ± 25 g; 100 μM: MAP = 14 ± 4 mmHg, HR = 16 ± 5 beats/min, tension = 330 ± 34 g). Preadministration of an opioid antagonist, naloxone (100 μM), augmented contraction-evoked MAP and HR responses and blocked effects of 100 μM DAME. Microdialysis of DAME into the cVLM produced no changes in the pressor response to contraction. At end of each experiment, tibial nerve stimulation after neuromuscular blockade evoked no MAP or HR change. Results demonstrate that opioid receptor activation within the rVLM modulates cardiovascular responses to isometric muscle contraction.

Central 5-HT1A modulation of cardiovascular responses to tibial nerve stimulation-evoked muscle contraction

1997 ◽  
Vol 272 (4) ◽  
pp. R1020-R1027 ◽  
Author(s):  
A. Ally ◽  
D. Caringi ◽  
D. M. Koester ◽  
T. Kobayashi ◽  
D. J. Mokler
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Muscle Tension ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Motor Threshold ◽  
Tibial Nerve Stimulation ◽  
Prior Administration ◽  
Stimulation Of

The effects of administering 8-hydroxy-2-(di-n-propylamine) tetralin [8-OH-DPAT, a serotonin 1A (5-HT1A) receptor agonist] into the rostral ventrolateral medulla (RVLM) on cardiovascular responses during tibial nerve stimulation-evoked muscle contraction were investigated using anesthetized rats. Stimulation of the tibial nerve (3 times motor threshold, 0.1 ms, 40 Hz) for 30 s increased mean arterial pressure (MAP), heart rate (HR), and muscle tension by 25 +/- 3 mmHg, 24 +/- 4 beats/min, and 299 +/- 35 g, respectively. Bilateral microdialysis of 8-OH-DPAT (10 mM) for 30 min attenuated the stimulation-evoked increases in MAP (8 +/- 2 mmHg) and HR (11 +/- 5 beats/min), without a change in muscle tension (292 +/- 30 g). However, administration of 1 mM 8-OH-DPAT had no effect on the cardiovascular responses. Thirty minutes of microdialysis of 8-OH-DPAT (10 mM) into the caudal ventrolateral medulla produced no effect on cardiovascular responses during muscle contraction. Prior administration of 10 mM 1-[2-methoxyphenyl]-4-[4-(2-phthalimido)-butyl]piperazine (NAN-190), a 5-HT1A receptor antagonist, for 30 min into the RVLM blocked the attenuating effects of subsequent microdialysis of 8-OH-DPAT (10 mM). Results suggest that activation of 5-HT1A receptors within the RVLM inhibit cardiovascular responses elicited during static muscle contraction.

Extracellular serotonin changes in VLM during muscle contraction: effects of 5-HT1A-receptor activation

1997 ◽  
Vol 273 (6) ◽  
pp. H2899-H2909 ◽  
Author(s):  
Gudbjorn Asmundsson ◽  
Daryl Caringi ◽  
David J. Mokler ◽  
Toshio Kobayashi ◽  
Takeshi Ishide ◽  
...  
Keyword(s):  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Tibial Nerve ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Ventrolateral Medulla ◽  
Muscle Paralysis ◽  
Arterial Blood ◽  
Tibial Nerve Stimulation ◽  
Static Contraction

This study determined whether muscle contraction causes an increase in extracellular levels of serotonin (5-HT) in the rostral (rVLM) or caudal ventrolateral medulla (cVLM) in anesthetized rats. Muscle contraction, evoked by tibial nerve stimulation, increased mean arterial blood pressure (MAP) by 27 ± 4 mmHg ( n = 8). In addition, 5-HT levels in the rVLM were elevated by 65 ± 9% during the contraction ( n = 8). Results were similar over two repeated contractions. In contrast, muscle contraction increased MAP, but not 5-HT, levels in the cVLM ( n = 6). Tibial nerve stimulation after muscle paralysis had no effect on either MAP or 5-HT levels in both rVLM and cVLM. Microdialysis of a 5-HT1A agonist, 8-OH-DPAT (10 mM), into the rVLM for 30 min ( n = 6) blunted the MAP change and reduced 5-HT release during contraction. Administration of NAN-190, a 5-HT1A antagonist, into the rVLM had no effect on 5-HT release and cardiovascular responses during muscle contraction and blocked the changes in 5-HT, MAP, and heart rate to static contraction after subsequent microdialysis of 8-OH-DPAT. Results demonstrate that 5-HT levels in the rVLM increase during muscle contraction and that 5-HT1A-receptor activation in the rVLM blunts MAP response to muscle contraction via a decrease in the extracellular concentration of 5-HT.

scholarly journals Does long-term experimental antiorthostasis lead to cardiovascular deconditioning in the rat?

2009 ◽  
pp. 57-67
Author(s):  
G Raffai ◽  
C Csekő ◽  
L Kocsis ◽  
L Dézsi ◽  
E Monos
Keyword(s):  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Physiological Adaptation ◽  
Arterial Blood ◽  
Cardiovascular Deconditioning ◽  
Before And After ◽  
Head Up Tilt ◽  
Spontaneous Baroreflex

Microgravity or simulated microgravity induces acute and chronic cardiovascular responses, whose mechanism is pivotal for understanding of physiological adaptation and pathophysiological consequences. We investigated hemodynamic responses of conscious Wistar rats to 45º head-down tilt (HDT) for 7 days. Arterial blood pressure (BP) was recorded by telemetry. Heart rate (HR), spectral properties and the spontaneous baroreflex sensitivity (sBRS) were calculated. Head-up tilt (HUT) was applied for 2 h before and after HDT to assess the degree of any possible cardiovascular deconditioning. Horizontal control BP and HR were 112.5±2.8 mmHg and 344.7±10 bpm, respectively. HDT elicited an elevation in BP and HR by 8.3 % and 8.8 %, respectively, in less than 1 h. These elevations in BP and HR were maintained for 2 and 3 days, respectively, and then normalized. Heart rate variability was unchanged, while sBRS was permanently reduced from the beginning of HDT (1.01±0.08 vs. 0.74±0.05 ms/mmHg). HUT tests before and after HDT resulted in BP elevations (6.9 vs. 11.6 %) and sBRS reduction (0.44 vs. 0.37 ms/mmHg), respectively. The pressor response during the post-HDT HUT test was accompanied by tachycardia (13.7 %). In conclusion, chronic HDT does not lead to symptoms of cardiovascular deconditioning. However the depressed sBRS and tachycardic response seen during the post-HDT HUT test may indicate disturbances in cardiovascular control.

Antagonism of adenosine A1 receptors in the NTS does not affect the chemoreflex in awake rats

2001 ◽  
Vol 281 (6) ◽  
pp. R2072-R2078 ◽  
Author(s):  
Patrícia M. de Paula ◽  
Benedito H. Machado
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Pressor Response ◽  
Potassium Cyanide ◽  
Cardiovascular Responses ◽  
Baseline Heart Rate ◽  
Lateral Aspect ◽  
Adenosine A1 ◽  
Before And After ◽  
Awake Rats

The possible involvement of adenosine A1 receptors in neurotransmission of the sympathoexcitatory component of the chemoreflex in the nucleus tractus solitarii (NTS) of awake rats was evaluated. Unilateral microinjection of increasing doses of adenosine (0.01, 0.06, 0.12, 1.25, 2.5, and 5.0 nmol/50 nl) into the lateral aspect of the commissural NTS produced a long-lasting increase in baseline mean arterial pressure (MAP) and no changes in baseline heart rate (HR). Microinjection of adenosine at 1.25 nmol/50 nl (ED50) into the NTS ( n = 9) produced a significant increase in baseline MAP (119 ± 3, 122 ± 4, and 117 ± 4 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 ± 3 mmHg) but no significant changes after previous microinjection of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1 receptor antagonist (107 ± 3, 107 ± 3, and 106 ± 3 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 ± 3 mmHg). Microinjection of adenosine before and after DPCPX into the same site of the lateral commissural NTS produced no changes in baseline HR. In another group of rats ( n = 8), microinjection of DPCPX (0.285 nmol/50 nl) into lateral and midline aspects of the commissural NTS produced no significant changes in pressor (+46 ± 4 vs. +47 ± 2 mmHg) or bradycardic responses (−216 ± 9 vs. −226 ± 12 beats/min) to chemoreflex activation with intravenous potassium cyanide compared with control responses. These data show that microinjection of adenosine into the NTS produced a small and long-lasting pressor response by activating A1 receptors and that blockade of these receptors produced no changes in cardiovascular responses to chemoreflex activation. We conclude that adenosine A1 receptors are not involved in processing of the chemoreflex afferents at the NTS level.

Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves

1995 ◽  
Vol 268 (6) ◽  
pp. R1464-R1471 ◽  
Author(s):  
P. Ruggeri ◽  
R. Ermirio ◽  
C. Molinari ◽  
F. R. Calaresu
Keyword(s):  
Nerve Stimulation ◽  
Sural Nerve ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Electrolytic Lesions ◽  
Cardiovascular Neurons ◽  
Muscle Nerve ◽  
Stimulation Of

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.

Effects of angiotensin II on autonomic components of nasopharyngeal stimulation in male conscious rabbits

2005 ◽  
Vol 98 (5) ◽  
pp. 1607-1611 ◽  
Author(s):  
Tarek M. Mousa ◽  
Lie Gao ◽  
Kurtis G. Cornish ◽  
Irving H. Zucker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Cigarette Smoke ◽  
Pressor Response ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Ang Ii ◽  
Before And After ◽  
Conscious Rabbits

Angiotensin II (ANG II) is known to activate central sympathetic neurons. In this study we determined the effects of ANG II on the autonomic components of the cardiovascular responses to stimulation of nasopharyngeal receptors with cigarette smoke. Experiments were carried out in conscious New Zealand White rabbits instrumented to record arterial pressure and heart rate. Rabbits were exposed to 50 ml of cigarette smoke before and after subcutaneous osmotic minipump delivery of ANG II at a dose of 50 ng·kg−1·min−1 for 1 wk in one group and intracerebroventricular (icv) infusion at a dose of 100 pmol/min for 1 h in a second group. The responses were compared before and after heart rate was controlled by pacing. Autonomic components were evaluated by intravenous administration of atropine methyl bromide (0.2 mg/kg) and prazosin (0.5 mg/kg). ANG II given either systemically or icv significantly blunted the pressor response to smoke ( P < 0.05) when the bradycardic response was prevented. This blunted response was not due to an absolute increase in baseline blood pressure after ANG II infusion (71.64 ± 11.6 vs. 92.1 ± 19.8 mmHg; P < 0.05) because normalization of blood pressure with sodium nitroprusside to pre-ANG II levels also resulted in a significantly blunted pressor response to smoke. The effect of smoke was α1-adrenergic receptor-mediated because it was essentially abolished by prazosin in both the pre- and the post-ANG II states ( P < 0.05). These results suggest that elevations in central ANG II reduce the sympathetic response to smoke in conscious rabbits. This effect may be due to an augmentation of baseline sympathetic outflow and a reduction in reflex sensitivity similar to the effect of ANG II on baroreflex function.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

1991 ◽  
Vol 260 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
M. K. Bazil ◽  
F. J. Gordon
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Nmda Receptors ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Pressor Responses

These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.

Effect of sleep restriction on orthostatic cardiovascular control in humans

2000 ◽  
Vol 88 (3) ◽  
pp. 966-972 ◽  
Author(s):  
N. K. Muenter ◽  
D. E. Watenpaugh ◽  
W. L. Wasmund ◽  
S. L. Wasmund ◽  
S. A. Maxwell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Lower Body Negative Pressure ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Sleep Restriction ◽  
Orthostatic Tolerance ◽  
Arterial Baroreflex ◽  
Finger Arterial Pressure ◽  
Before And After

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction ( P > 0.3). Systolic pressure was greater at −60 mmHg LBNP after sleep restriction than before sleep restriction (110 ± 6 and 124 ± 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 ± 8 and 99 ± 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

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