Attenuating effects of intrathecal clonidine on the exercise pressor reflex

1991 ◽  
Vol 70 (2) ◽  
pp. 516-522 ◽  
Author(s):  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Arterial Pressure ◽  
Intrathecal Injection ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Ventilatory Responses ◽  
Exercise Pressor Reflex ◽  
Adrenergic Antagonist ◽  
Anesthetic Action ◽  
Intrathecal Clonidine ◽  
Stimulation Of

We tested the hypothesis that intrathecal injection of clonidine, an alpha 2-adrenergic agonist, attenuated the reflex cardiovascular and ventilatory responses to static muscular contraction in cats. Before clonidine (1 microgram in 0.2 ml), contraction-induced reflex increases (n = 10) in mean arterial pressure and ventilation averaged 25 +/- 3 mmHg and 359 +/- 105 ml/min, respectively, whereas after clonidine these increases averaged 8 +/- 4 mmHg and 200 +/- 114 ml/min, respectively (P less than 0.05). Clonidine had no effect on the heart rate response to contraction. Intrathecal injection of yohimbine (10 micrograms; n = 5), an alpha 2-adrenergic antagonist, but not prazosin (10 micrograms; n = 3), an alpha 1-adrenergic antagonist, prevented the attenuating effects of clonidine on the reflex pressor and ventilatory responses to contraction. Our findings were not due to the spread of clonidine to the medulla, because the reflex pressor and ventilatory responses to contraction were not attenuated by injection of clonidine (1 microgram) onto the medulla (n = 3). In addition, our findings were not due to a clonidine-induced withdrawal of sympathetic outflow, because intrathecal injection of clonidine (1 microgram) did not attenuate increases in arterial pressure and ventilation evoked by high-intensity electrical stimulation of the cut central end of the sciatic nerve (n = 5). Furthermore, our findings were not due to a local anesthetic action of clonidine, because application of this agent to the dorsal roots had no effect on the discharge of group IV muscle afferents. We conclude that stimulation of alpha 2-adrenergic receptors in the spinal cord attenuates the reflex pressor and ventilatory responses to static contraction.

Attenuation of reflex pressor and ventilatory responses to static muscular contraction by intrathecal opioids

1990 ◽  
Vol 68 (6) ◽  
pp. 2466-2472 ◽  
Author(s):  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Opioid Peptides ◽  
Intrathecal Injection ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Reflex Responses ◽  
Ventilatory Responses ◽  
Static Contraction

We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 micrograms in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 +/- 5 (SE) mmHg and 227 +/- 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 +/- 5 mmHg and 37 +/- 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P less than 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid mu- or delta-receptor attenuated the reflex responses to static contraction. Naloxone (1,000 micrograms), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.

Attenuation of reflex pressor and ventilatory responses to static contraction by an NK-1 receptor antagonist

1992 ◽  
Vol 73 (4) ◽  
pp. 1389-1395 ◽  
Author(s):  
J. M. Hill ◽  
J. G. Pickar ◽  
M. P. Kaufman
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Receptor Antagonist ◽  
Dorsal Horn ◽  
Intrathecal Injection ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Neurokinin A ◽  
Ventilatory Responses ◽  
Static Contraction

The chemical messengers released onto second-order dorsal horn neurons from the spinal terminals of contraction-activated group III and IV muscle afferents have not been identified. One candidate is the tachykinin substance P. Related to substance P are two other tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which, like substance P, have been isolated in the dorsal horn of the spinal cord and have receptors there. Whether NKA or NKB plays a transmitter/modulator role in the spinal processing of the exercise pressor reflex is unknown. Therefore, we tested the following hypotheses. After the intrathecal injection of a highly selective NK-1 (substance P) receptor antagonist onto the lumbosacral spinal cord, the reflex pressor and ventilatory responses to static muscular contraction will be attenuated. Likewise, after the intrathecal injection either of an NK-2 (NKA) receptor antagonist or an NK-3 (NKB) receptor antagonist onto the lumbrosacral spinal cord, the reflex pressor and ventilatory responses to static contraction will be attenuated. We found that, 10 min after the intrathecal injection of 100 micrograms of the NK-1 receptor antagonist, the pressor and ventilatory responses to contraction were significantly (P < 0.05) attenuated. Mean arterial pressure was attenuated by 13 +/- 3 mmHg (48%) and minute volume of ventilation by 120 +/- 38 ml/min (34%). The cardiovascular and ventilatory responses to contraction before either 100 micrograms of the NK-2 receptor antagonist or 100 micrograms of the NK-3 receptor antagonist were not different (P > 0.05) from those after the NK-2 or the NK-3 receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of peripheral and spinal κ-opioid receptor stimulation on the exercise pressor reflex in decerebrate rats

2014 ◽  
Vol 307 (3) ◽  
pp. R281-R289 ◽  
Author(s):  
Steven W. Copp ◽  
Audrey J. Stone ◽  
Katsuya Yamauchi ◽  
Marc P. Kaufman
Keyword(s):  
Opioid Receptor ◽  
Opioid Receptors ◽  
Pressor Response ◽  
Intrathecal Injection ◽  
Muscle Afferents ◽  
Femoral Arteries ◽  
Exercise Pressor Reflex ◽  
Pressor Responses ◽  
Pressor Reflex ◽  
Stimulation Of

The exercise pressor reflex is greater in rats with ligated femoral arteries than it is in rats with freely perfused femoral arteries. The exaggerated reflex in rats with ligated arteries is attenuated by stimulation of μ-opioid and δ-opioid receptors on the peripheral endings of thin-fiber muscle afferents. The effect of stimulation of κ-opioid receptors on the exercise pressor reflex is unknown. We tested the hypothesis that stimulation of κ-opioid receptors attenuates the exercise pressor reflex in rats with ligated, but not freely perfused, femoral arteries. The pressor responses to static contraction were compared before and after femoral arterial or intrathecal injection of the κ-opioid receptor agonist U62066 (1, 10, and 100 μg). Femoral arterial injection of U62066 did not attenuate the pressor responses to contraction in either group of rats. Likewise, intrathecal injection of U62066 did not attenuate the pressor response to contraction in rats with freely perfused femoral arteries. In contrast, intrathecal injection of 10 and 100 μg of U62066 attenuated the pressor response to contraction in rats with ligated femoral arteries, an effect that was blocked by prior intrathecal injection of the κ-opioid receptor antagonist nor-binaltorphimine. In rats with ligated femoral arteries, the pressor response to stimulation of peripheral chemoreceptors by sodium cyanide was not changed by intrathecal U62066 injections, indicating that these injections had no direct effect on the sympathetic outflow. We conclude that stimulation of spinal, but not peripheral, κ-opioid receptors attenuates the exaggerated exercise pressor reflex in rats with ligated femoral arteries.

Inhibition of aortic chemoreceptor discharge by pressor response to muscular contraction

1987 ◽  
Vol 62 (6) ◽  
pp. 2258-2263
Author(s):  
K. W. McCoy ◽  
D. M. Rotto ◽  
M. P. Kaufman
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Pressure Response ◽  
Hindlimb Muscles ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Static Contraction

We have examined the effect of static contraction of the hindlimb muscles on the discharge of aortic chemoreceptors in chloralose-anesthetized cats. The responses of the chemoreceptors to contraction were dependent on the arterial pressure response to this maneuver. When contraction reflexly evoked a pressor response of at least 20 mmHg, the discharge of 26 chemoreceptors was reduced from control levels by 53% (P less than 0.01). The contraction-induced inhibition of chemoreceptor discharge was prevented by phentolamine, an alpha-adrenergic antagonist that also attenuated the contraction-induced pressor response. In addition, the inhibition evoked by contraction was simulated by injection of phenylephrine and inflation of an aortic balloon, both of which evoked pressor responses. However, when contraction failed to significantly change arterial pressure, the discharge of 20 aortic chemoreceptors was not significantly changed from control levels. We conclude that the reflex pressor response to static contraction inhibits the discharge of aortic chemoreceptors. This inhibition of discharge needs to be considered when interpreting the effects of aortic barodenervation on the cardiovascular responses to exercise.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Spinal vasopressin mechanisms of cardiovascular regulation

1986 ◽  
Vol 251 (3) ◽  
pp. R510-R517 ◽  
Author(s):  
J. P. Porter ◽  
M. J. Brody
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Neural Control ◽  
Intrathecal Injection ◽  
Cardiovascular Regulation ◽  
Spinal Subarachnoid Space ◽  
Vascular Beds ◽  
Vasopressinergic Neurons ◽  
Stimulation Of ◽  
Related Increase

Extrahypothalamic vasopressin-containing neurons have been implicated in the central neural control of the cardiovascular system. In the present study we investigated the possibility that vasopressinergic neurons arising from the paraventricular nucleus (PVN) and terminating in the spinal cord are involved in the regulation of vasomotor functions. Vasopressin (1-17 pmol) was injected into the spinal subarachnoid space of conscious rats instrumented with Doppler flow probes and indwelling intrathecal catheters. The peptide produced a dose-related increase in arterial pressure accompanied by vasoconstriction in the mesenteric, renal, and hindquarter vascular beds. Pretreatment, intrathecally, with 0.5 nmol of the vasopressin antagonist d(CH2)5Me(Tyr)AVP completely prevented the increase in arterial pressure expected after subsequent intrathecal injection of vasopressin. However, the changes in arterial pressure and vascular resistances produced by stimulation of the PVN were not affected by the intrathecal antagonist. Stimulation of the PVN in Brattleboro rats, which lack hypothalamic and spinal vasopressin, produced hemodynamic responses similar to those produced in Long-Evans control rats. Taken together, these data suggest that spinal vasopressin can act within the spinal cord to alter vasomotor functions; however, the hemodynamic effects evoked by stimulation of the PVN do not appear to depend on spinal vasopressinergic mechanisms.

Effects of hindlimb contraction on pressor and muscle interstitial metabolite responses in the cat

1998 ◽  
Vol 85 (4) ◽  
pp. 1583-1592 ◽  
Author(s):  
Dave A. MacLean ◽  
Kathryn F. LaNoue ◽  
Kristen S. Gray ◽  
Lawrence I. Sinoway
Keyword(s):  
Muscle Afferents ◽  
Decerebrate Cat ◽  
Exercise Pressor Reflex ◽  
Interstitial Concentration ◽  
Pressor Responses ◽  
Pressor Reflex ◽  
Lactate Levels ◽  
First Time ◽  
Made In ◽  
Stimulation Of

We used the microdialysis technique to measure the interstitial concentration of several putative metabolic stimulants of the exercise pressor reflex during 3- and 5-Hz twitch contractions in the decerebrate cat. The peak increases in heart rate and mean arterial pressure during contraction were 20 ± 5 beats/min and 21 ± 8 mmHg and 27 ± 9 beats/min and 37 ± 12 mmHg for the 3- and 5-Hz stimulation protocols, respectively. All variables returned to baseline after 10 min of recovery. Interstitial lactate rose ( P < 0.05) by 0.41 ± 0.15 and 0.56 ± 0.16 mM for the 3- and 5-Hz stimulation protocols, respectively, and were not statistically different from one another. Interstitial lactate levels remained above ( P < 0.05) baseline during recovery in the 5-Hz group. Dialysate phosphate concentrations (corrected for shifts in probe recovery) rose with stimulation ( P < 0.05) by 0.19 ± 0.08 and 0.11 ± 0.03 mM for the 3- and 5-Hz protocols. There were no differences between groups. The resting dialysate K+ concentrations for the 3- and 5-Hz conditions were 4.0 ± 0.1 and 3.9 ± 0.1 meq/l, respectively. During stimulation the dialysate K+ concentrations rose steadily for both conditions, and the increase from rest to stimulation ( P < 0.05) was 0.57 ± 0.19 and 0.81 ± 0.06 meq/l for the 3- and 5-Hz conditions, respectively, with no differences between groups. Resting dialysate pH was 6.915 ± 0.055 and 6.981 ± 0.032 and rose to 7.013 ( P < 0.05) and 7.053 ( P < 0.05) for the 3- and 5-Hz conditions, respectively, and then became acidotic (6.905, P < 0.05) during recovery (5 Hz only). This study represents the first time simultaneous measurements of multiple skeletal muscle interstitial metabolites and pressor responses to twitch contractions have been made in the cat. These data suggest that interstitial K+ and phosphate, but not lactate and H+, may contribute to the stimulation of thin fiber muscle afferents during contraction.

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits

2000 ◽  
Vol 278 (3) ◽  
pp. H871-H877 ◽  
Author(s):  
J. M. Legramante ◽  
G. Raimondi ◽  
C. M. Adreani ◽  
S. Sacco ◽  
F. Iellamo ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Muscle Twitch ◽  
Group Iii ◽  
Twitch Contraction ◽  
Depressor Response ◽  
Stimulation Of

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

scholarly journals Role of Muscular Contraction in the Reflex Vascular Responses to Stimulation of Muscle Afferents in the Dog

1973 ◽  
Vol 33 (4) ◽  
pp. 386-392 ◽  
Author(s):  
DENIS L. CLEMENT ◽  
CONRAD L. PELLETIER ◽  
JOHN T. SHEPHERD
Keyword(s):  
Muscular Contraction ◽  
Muscle Afferents ◽  
Vascular Responses ◽  
Stimulation Of
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